ObjectiveThe comparative effectiveness of various mind-body exercises for chronic obstructive pulmonary disease remains unclear. This study aimed to compare and rank different mind-body interventions for improving objective and subjective outcomes in patients with chronic obstructive pulmonary disease.Data sourcesWe systematically searched PubMed, Web of Science, EMBASE, Cochrane Library, and Scopus.MethodsRandomised controlled trials assessing mind-body exercises for chronic obstructive pulmonary disease were included. A network meta-analysis was performed using Stata 16.0. The protocol was registered with PROSPERO (CRD42024592835).ResultsThirty-seven studies involving 3179 participants and nine interventions were analysed. Regarding objective outcomes, Pilates plus pulmonary rehabilitation showed the largest improvement in exercise capacity. For pulmonary function, Pilates plus pulmonary rehabilitation significantly improved forced expiratory volume in the first second as a percentage of the predicted value and forced expiratory volume in the first second/forced vital capacity, while Yoga demonstrated superior effects on forced expiratory volume in the first second and forced vital capacity. Regarding subjective outcomes, Tai Chi, alone or combined with pulmonary rehabilitation, was superior in reducing dyspnea, while Tai Chi plus pulmonary rehabilitation and Qigong showed the greatest benefits for health-related quality of life.ConclusionsMind-body exercises are beneficial for chronic obstructive pulmonary disease management. Pilates plus pulmonary rehabilitation stands out for improving objective outcomes, particularly exercise capacity and pulmonary function, whereas Tai Chi, alone or combined with pulmonary rehabilitation, emerges as the most effective intervention for subjective outcomes, including dyspnea and health-related quality of life.

BackgroundDiaphragmatic dysfunction contributes to exercise intolerance in COPD, but whether BMI shapes baseline function and response to exercise remains unclear. This secondary analysis characterized BMI-related diaphragmatic phenotypes and whether diaphragm thickening fraction (TFdi) links exercise training to functional improvement.MethodsData were analyzed from 103 patients with stable COPD in a completed 2×2 factorial randomized trial. Because no exercise-by-acupuncture interaction was detected for 4-week TFdi, participants were regrouped as exercise-exposed or non-exercise. Associations between BMI and baseline TFdi were assessed using restricted cubic splines and threshold models. Regression models estimated exercise effects on 4-week TFdi and 6-minute walk distance (6MWD), with BMI-stratified interaction and exploratory mediation analyses.ResultsBMI showed a nonlinear association with baseline TFdi, with an adjusted turning point at 23.7 kg/m². Below this threshold, BMI was positively associated with TFdi (β=0.05, 95% CI 0.03–0.08); above it, the association was negative (β=−0.05, 95% CI −0.07 to −0.03). Exercise was associated with higher 4-week TFdi (β=0.15, 95% CI 0.01–0.29) and longer 6MWD (β=59.61 m, 95% CI 10.65–108.57). The TFdi response was most pronounced at BMI ≥25.0 kg/m², with borderline interaction evidence. Exploratory mediation suggested TFdi partially mediated exercise-related 6MWD gains, particularly in this BMI group.ConclusionsThis study integrates BMI phenotyping, diaphragm ultrasound, and mediation analysis to show that diaphragmatic function and exercise-induced diaphragmatic adaptation in COPD are BMI dependent. BMI may help identify patients most likely to derive diaphragmatic benefit from rehabilitation.

Objectives: The current study examined whether exercise training alleviates cigarette smoke (CS)-induced diaphragm dysfunction by modulating inflammation through the Wnt and Chemerin signaling pathways. Methods: Mechanical stretching was applied for 3 consecutive days to explore the effects on cell proliferation and chemerin/chemokine-like receptor 1 (CMKLR1) expression in C2C12 cells pretreated with lipopolysaccharide. Male wild-type (WT) and CMKLR1 knockout (KO) mice (6-8 weeks old) were exposed to CS for 6 months (1-2 h a day, 6 days a week) to determine the role of chemerin/CMKLR1 in the progression of diaphragm dysfunction. Given that Wnt/β-catenin is a potential modulator of chemerin/CMKLR1, its expression was detected in CS-exposed mice and mice subjected to treadmill exercise training after CS exposure. Wnt/β-catenin agonist lithium chloride (LiCl) and antagonist XAV939 were then intraperitoneally injected into the CS-exposed mice during exercise training to further investigate their potential synergistic effects with exercise training on improving CS-induced diaphragm dysfunction. Isolated diaphragm contraction strength and fiber cross-sectional area were measured to determine the diaphragm dysfunction. Results: Mechanical stretching improved the proliferation level of myoblasts and decreased inflammation and CMKLR1 protein expression (p < 0.05). The KO mice showed diminished diaphragm dysfunction compared with the WT mice after long-term CS exposure. Combined LiCl and exercise training further enhanced the improvement of diaphragmatic isolated strength in mice exposed to CS (p < 0.01), activated the protein degradation and synthesis pathways, and decreased IL-1β level (p < 0.05). Combined XAV939 and exercise training significantly decreased chemerin protein level (p < 0.01). Conclusions: Exercise training can downregulate inflammation levels and improve diaphragm dysfunction in CS-exposed mice, partially by enhancing Wnt expression and reducing abnormally activated chemerin.

Chronic obstructive pulmonary disease (COPD) ranks among the leading causes of global mortality, with chronic inflammation as its primary pathogenic mechanism. Developing effective therapeutic strategies to attenuate this inflammatory response is crucial for reducing the prevalence, mortality, and overall burden of COPD. Polyunsaturated fatty acids (PUFAs) are recognized for their role in modulating inflammation and may influence inflammation-driven diseases. This narrative review evaluates observational and interventional studies on PUFAs in COPD and explores their potential mechanisms in modulating inflammation. The synthesis of the literature reveals limited and inconsistent evidence linking PUFAs to COPD. Robust data are lacking to conclusively demonstrate the biological benefits and clinical efficacy of n-3 PUFAs in COPD. Therefore, we systematically assess current research and recommends extensive and rigorous future clinical trials. Furthermore, PUFAs and their derivatives play roles in initiating and resolving inflammation in COPD through direct involvement, macrophage polarization regulation, and effects on membrane biophysics and signal transduction. Despite the current inconclusive evidence, we emphasize the necessity for intensified clinical trials and drug development efforts targeting PUFAs in COPD to develop new therapeutic strategies.

Background and aimCOPD is a common respiratory disease characterized by progressive airflow restriction that severely affects patients' quality of life and leads to significant mortality rates worldwide. This study aims to strengthen the early diagnosis of COPD and develop personalized treatment strategies.MethodsThe methodology involved a comprehensive approach, including differential gene expression analysis, weighted gene co-expression network analysis (WGCNA), functional enrichment analysis, and machine learning techniques. Data from the combined datasets GSE37768 and GSE38974 were utilized to identify differentially expressed genes (DEGs). The machine learning integrated model was employed to screen for diagnostic molecular biomarkers related to COPD. Additionally, pathway analysis, transcription factor gene regulatory network analysis, immune cell composition analysis using CIBERSORT, and mendelian randomization analysis were conducted to elucidate the molecular mechanisms and potential biomarkers for COPD. Finally, we validated the model using Polymerase Chain Reaction (PCR), immunohistochemistry (IHC) and Immunofluorescence (IF).ResultsThis study employed bioinformatics and Integrated Machine Learning Methods to identify ITGB2 and HNRNPAB as potential related targets for COPD. Subsequent verification through PCR, IHC, and IF experiments confirmed that ITGB2 and HNRNPAB were key biomarkers for COPD. Pathway analysis revealed that ITGB2 and HNRNPAB were mainly involved in immune responses and metabolic pathways.ConclusionThis comprehensive study presents an in-depth investigation of the molecular mechanisms of COPD and identifies candidate exploratory biomarkers for further research toward early diagnosis and potential personalized treatment strategies. In future studies, the identified exploratory biomarkers should be validated in larger cohorts and their therapeutic significance explored.

Chronic obstructive pulmonary disease (COPD), characterized by persistent airflow limitation and chronic inflammation, still lacks therapies that truly modify the disease course. Emerging studies suggest that lipophagy may occupy a pivotal position in pulmonary and systemic lipid homeostasis in COPD. This review aims to integrate evidence regarding how lipophagy reshapes cellular metabolism and interfaces with canonical pathogenic processes in COPD, and to evaluate its translational prospects. We delineate, in the context of COPD, the links between lipophagy and glycolysis, fatty-acid β-oxidation, lipid synthesis and catabolism, and mitochondrial function. In this narrative review, we integrate and critically discuss evidence on how lipophagy reshapes cellular metabolism and interfaces with canonical pathogenic processes in COPD. We summarize mechanistic links between lipophagy imbalance and lipid-droplet accumulation, inflammation and immune responses, oxidative stress and proteostasis disruption, apoptosis, and cellular senescence, and we discuss extra-pulmonary manifestations including skeletal-muscle fat infiltration and satellite-cell dysfunction. We posit that lipophagy resides at the intersection of metabolism, organelle quality control, and inflammatory signaling in COPD; "calibrated reconstruction" of lipophagy may re-establish bioenergetics and mitigate lipotoxicity, thereby offering a new perspective for developing lipophagy-based interventions to improve COPD progression.

Transcranial direct current stimulation (tDCS) positively affects post-stroke cognitive impairment (PSCI). However, the optimal stimulation protocol remains unclear, possibly because of the lack of objective assessment methods. Therefore, this study aims to investigate the impact of tDCS on the modulation of the excitation/inhibition (E/I) balance and its effects on brain function in patients with PSCI using transcranial magnetic stimulation (TMS) and functional near-infrared spectroscopy (fNIRS). This study is a single-centre, two-armed randomised controlled trial. A total of 40 patients with PSCI will be recruited and randomly assigned to real and sham tDCS groups in a 1:1 ratio. Both groups will receive either real or sham tDCS in addition to conventional treatment. In both groups, electrodes will be placed at the same positions, with the anode and cathode above the left and right dorsolateral prefrontal cortex, respectively. The real tDCS group will receive continuous current throughout the session, whereas the sham tDCS group will receive current generation for only the first 30 s. The treatment will consist of a 3-week intervention with one session per day, five sessions per week and 30 min per session. A 4-week follow-up will be conducted at the end of the treatment. The primary outcome is the change in Montreal cognitive assessment (MoCA) scores from baseline (T0) to immediately post-intervention (T1). Secondary outcomes include Barthel index, levels of intracortical inhibition measured by TMS and cortical activation and interhemispheric connectivity assessed by fNIRS during a Stroop task. This study will combine TMS and fNIRS to explore the effects of tDCS on the modulation of the E/I balance and its impact on blood oxygen levels and neural activity. Our results are expected to provide a clinical reference for the development of more precise tDCS protocols. Chinese Clinical Trials Registry ChiCTR2300077453. Registered on November 9, 2023.

Background:Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death worldwide, of which 41.27% of the burden may be related to particulate matter (PM) pollution. Understanding the PM-related burden of COPD at global, national and regional levels can provide evidence for public health policies. Methods:First, the numbers of death and disability-adjusted life year (DALY), and the corresponding age-standardized rates were assessed globally and by subtype, including age, sex, sociodemographic index (SDI), country, and region from 1990 to 2021. Second, the temporal trend in disease burden was estimated by joinpoint regression analysis. Furthermore, an international health inequality analysis was used to assess the inequality slope indices and concentration indices, and frontier analysis was performed to explore the current situation and potential improvement of disease burden control. Finally, we constructed an auto regressive integrated moving average model to predict PM-related burden of COPD in the next 15 years. Results:In 2021, the number of COPD deaths and DALYs attributed to PM were approximately 1.54 million and 33.24 million, respectively. The age-standardized death rate (ASMR) and age-standardized DALY rate (ASDR) were 1.66 and 1.50 times higher in males than in females. Interestingly, the ASMR and ASDR exhibited an increase from 2020 to 2021. The highest COPD burden attributed to PM was in low and low-middle SDI regions. Countries with an SDI between 0.3 and 0.6 had the greatest potential to reduce the COPD burden attributed to PM, especially in Asia, Oceania, and Africa. In the next 15 years, the ASMR and ASDR of COPD attributable to PM for both sexes will decrease, and the difference between male and female patients will be almost nonexistent. Conclusion:The COPD burden attributable to PM remains a long-term problem globally, especially in males, the older adults, and low and low-middle SDI regions.

Chronic obstructive pulmonary disease (COPD) is frequently accompanied by skeletal muscle dysfunction, a critical and severe extrapulmonary complication. This dysfunction contributes to reduced exercise capacity, increased frequency of acute exacerbations, and elevated mortality, serving as an independent risk factor for poor prognosis in COPD patients. Owing to the unique physicochemical conditions of the marine environment, marine-derived bioactive compounds exhibit potent anti-inflammatory and antioxidant properties, demonstrating therapeutic potential for ameliorating COPD skeletal muscle dysfunction. This review summarizes marine-derived bioactive compounds with promising efficacy against skeletal muscle dysfunction in COPD, including polysaccharides, lipids, polyphenols, peptides, and carotenoids. The discussed compounds have shown bioactivities in promoting skeletal muscle health and suppressing muscle atrophy, thereby providing potential strategies for the prevention and treatment of COPD skeletal muscle dysfunction. These findings may expand the therapeutic strategies for managing COPD skeletal muscle dysfunction.

Chronic obstructive pulmonary disease (COPD), a major global cause of morbidity and mortality, is pathologically defined by persistent oxidative stress, chronic inflammation, and dysregulated cell death pathways. This review critically examines the emerging role of the transcription factor Nrf2 in modulating these processes within COPD, with particular emphasis on its potential regulation of ferroptosis, a novel iron-dependent form of regulated cell death implicated in disease pathogenesis. We explore the complex regulation of Nrf2, including both Keap1-dependent and -independent degradation mechanisms, as well as its upstream activators and downstream effectors in the context of COPD. Notably, we provide evidence that Nrf2 dysfunction weakens cellular defenses against oxidative stress and inflammation while increasing susceptibility to ferroptosis. Ferroptosis, marked by iron accumulation, glutathione (GSH) depletion, glutathione peroxidase 4 (GPX4) inactivation, and lipid peroxidation, is emerging as a key driver of airway epithelial damage, emphysema, and inflammation in COPD. We also delve into the molecular mechanisms of the Nrf2-ferroptosis axis, highlighting the role of Nrf2 in regulating iron homeostasis, the System Xc-/GSH/GPX4 pathway, and lipid peroxidation, with additional crosstalk to pathways like peroxisome proliferator-activated receptor gamma (PPARγ). These insights underscore the potential for targeting Nrf2-mediated ferroptosis in developing novel therapeutic approaches to combat COPD.

Dysfunctional mitochondrial quality control (MQC) and dysregulated programmed cell death (PCD) are increasingly recognized as key drivers of pulmonary diseases. This review explores the intricate crosstalk between MQC mechanisms, encompassing mitochondrial biogenesis, dynamics, mitophagy, and mitocytosis, and novel PCD pathways such as pyroptosis, ferroptosis, necroptosis, PANoptosis, cuproptosis, and disulfidptosis. We highlight how mitochondrial dysfunction triggers PCD and how PCD exacerbates mitochondrial damage, creating a vicious cycle that amplifies lung injury and inflammation. Emerging therapeutic strategies targeting these interconnected pathways show promise in mitigating pulmonary diseases. However, challenges remain in understanding the context-dependent roles and translating preclinical findings into clinical applications. Further research is still needed to elucidate the precise regulatory mechanisms governing MQC and PCD, identify novel therapeutic targets, and develop biomarkers for early disease detection and prognosis. This review underscores the potential of targeting MQC and PCD as a therapeutic direction for pulmonary diseases, offering new insights into disease pathogenesis and treatment.

Objective: This study examines the dose–response relationship between physical activity (PA) and all-cause mortality across different severities of airflow limitation, identifying threshold effects that yield new insights into the PA–mortality association. Design: A prospective cohort study with a 5-year follow-up (2018–2023), employing multivariate Cox models and penalized spline smoothing to assess non-linear associations. Subjects/Patients: A total of 2,975 individuals from a cohort categorized by airflow limitation severity (normal, GOLD 1–4). Methods: PA levels were quantified in metabolic equivalent hours per week (MET·h/week). Cox proportional hazards models were used to evaluate PA–mortality associations, with penalized spline analysis detecting threshold effects. Results: Identified thresholds were 41.50 MET·h/week (95% CI: 23.03–64.22) for normal lung function and 13.21 MET·h/week (95% CI: 9.67–16.14) for GOLD 1. Below these thresholds, higher PA levels were associated with a significant reduction in mortality risk (HR = 0.66, HR = 0.41, respectively). In GOLD 2, PA levels below the threshold were associated with a lower mortality risk (HR=0.85), whereas PA exceeding the threshold was associated with a higher mortality risk (HR = 1.23). No significant associations were observed in GOLD 3–4. Conclusion: PA demonstrates a non-linear, threshold-dependent association with mortality. These findings underscore the importance of individualized PA recommendations for optimizing health outcomes in individuals with chronic respiratory conditions.

Background:Pulmonary arterial hypertension (PAH) is a progressive disease associated with high fatality rate. Comprehensive evidence concerning the epidemiology of PAH mortality is lacking. The present study aimed to assess the mortality and trends of PAH at global, regional, and national levels from 1990 to 2021. Methods:The estimates and their 95% uncertainty interval for case number of PAH were collected from the Global Burden of Disease, Injuries, and Risk Factors Study (GBD) 2021. Age standardization by direct method was used to estimate the age-standardized mortality rate (ASMR) for PAH. We investigated the temporal trends of estimated ASMR from 1990 to 2021 and further predicted its changes in the next 15 years, decomposed the trends based on demographic factors and epidemiological changes, and quantified the cross-country health inequalities. Results:The global ASMR of PAH decreased from 0.35 (per 100,000 population) in 1990 to 0.27 (per 100,000 population) in 2021, with an annual percentage change of -0.82, while number of deaths increased from 14,842 in 1990 to 22,021 in 2021, an increase of 48.37%. Population growth and aging were the major drivers contributing to the number of deaths, accounting for 93.88% and 32.26%. Of note, there were significant health inequalities across 204 countries and territories, with the slope index of inequality rising over time. Projection of the global burden of PAH from 2022 to 2036 demonstrated a progressive increase in case number, but the ASMR remained largely unchanged. Conclusion:PAH remains a major public health concern in some regions, particularly in high sociodemographic index region. Adequate diagnosis and targeted treatment of PAH are urgently needed to achieve a reduction in mortality.

BackgroundChronic Obstructive Pulmonary Disease (COPD) is a leading cause of global mortality, characterized by chronic inflammation and abnormal immune responses in the lower airways. Recent studies have highlighted the critical role of immune function in the pathogenesis and progression of COPD. The disease is characterized by abnormal immune responses in the lower respiratory tract, with its progression associated with the infiltration of innate and adaptive inflammatory immune cells into the lungs and the formation of lymphoid follicles, mediated by cytokines and inflammasomes. Increasing evidence suggests that cell-mediated immunity has an important role in the pathogenesis of COPD, which is characterized by immune senescence leading to decreased resistance to infection, enhanced neutrophil and macrophage activation, T-cell infiltration, and aberrant B-cell activity, all of which combine to contribute to airway inflammation and lung injury in patients with COPD.ObjectiveThis review aimed to explore the pivotal role of the immune system in COPD and its therapeutic potential.MethodsWe reviewed, categorized, and summarized literature on immunity and COPD published in the last five years from Web of Science and PubMed databases.ResultsThis study elucidates the pivotal role of immune dysregulation in COPD pathogenesis, particularly the dysfunctional transition from innate to adaptive immunity. We delineate how specific immune cell populations—including macrophages, neutrophils, and T-lymphocytes—contribute to sustained airway inflammation and lung injury in COPD through aberrant activation, infiltration, and impaired function. Mechanistically, key features of this dysregulation involve aberrant cytokine signaling pathways and defective resolution of inflammation. These insights reveal potential therapeutic targets for immunomodulatory strategies aimed at interrupting the chronic inflammatory cascade, restoring immune homeostasis, and mitigating infection susceptibility in COPD. Promising approaches highlighted include targeting specific cytokines, modulating macrophage polarization states, and enhancing mucosal immune defenses.

Chronic obstructive pulmonary disease (COPD) and insomnia are highly comorbid, yet their shared pathogenesis and therapeutic targets remain unclear. This study employed multidimensional approaches—including bidirectional Mendelian randomization (MR), transcriptomic analysis, weighted gene co-expression network analysis (WGCNA), and computational drug repositioning—to investigate causal relationships, shared pathways, and therapeutic strategies for COPD–insomnia comorbidity. MR analysis indicated that insomnia is a causal risk factor for COPD (OR = 2.04, 95% CI: 1.18–3.51; p = 0.011), with no reverse causality. Integrated transcriptomics of COPD (GSE148004) and insomnia (GSE208668) identified 230 co-dysregulated genes enriched in immune-inflammatory pathways (e.g., NF-κB signaling and cytokine response) and oxidative stress. Protein–protein interaction networks highlighted TNFAIP3 as a hub gene, confirmed by LASSO regression as a shared diagnostic biomarker. A co-expression network of 190 overlapping genes linked circadian disruption and airway inflammation. Drug repositioning nominated TNFAIP3-targeting agents, and molecular docking revealed high-affinity binding between berbamine and the TNFAIP3 OTU domain (ΔG = −9.25 kcal/mol). TNFAIP3 emerges as a dual regulator of inflammatory signaling and redox homeostasis. Our systems pharmacology approach bridges epidemiological causality and molecular mechanisms, supporting single-agent polypharmacology for COPD–insomnia comorbidity.

Skeletal muscle dysfunction is a common extrapulmonary comorbidity of chronic obstructive pulmonary disease (COPD) and is associated with decreased quality-of-life and survival in patients. The autophagy lysosome pathway is one of the proteolytic systems that significantly affect skeletal muscle structure and function. Intriguingly, both promoting and inhibiting autophagy have been observed to improve COPD skeletal muscle dysfunction, yet the mechanism is unclear. This paper first reviewed the effects of macroautophagy and mitophagy on the structure and function of skeletal muscle in COPD, and then explored the mechanism of autophagy mediating the dysfunction of skeletal muscle in COPD. The results showed that macroautophagy- and mitophagy-related proteins were significantly increased in COPD skeletal muscle. Promoting macroautophagy in COPD improves myogenesis and replication capacity of muscle satellite cells, while inhibiting macroautophagy in COPD myotubes increases their diameters. Mitophagy helps to maintain mitochondrial homeostasis by removing impaired mitochondria in COPD. Autophagy is a promising target for improving COPD skeletal muscle dysfunction, and further research should be conducted to elucidate the specific mechanisms by which autophagy mediates COPD skeletal muscle dysfunction, with the aim of enhancing our understanding in this field.

Background Traditional Chinese exercises (TCEs), as a new technology for pulmonary rehabilitation, have been proven to be effective in patients with chronic obstructive pulmonary disease (COPD). However, further aggravation of dynamic hyperinflation manifested as exertional dyspnea during exercises may limit the partial therapeutic efficacy of TCEs on patients with COPD. Acupuncture therapy, internationally recognized as a complementary and alternative therapy, can effectively improve the degree of dyspnea, and it is expected to serve as an adjuvant therapy for exercise training in patients with COPD to fully realize the therapeutic efficacy of exercise training. Therefore, this study aims to explore the multidimensional and multi-system effects of the combination of pulmonary-based Qigong (PQ) exercise and acupuncture therapy on patients with COPD. Methods This protocol describes an assessor-blinded, data analyst-blinded, four-arm randomized controlled trial that aims to recruit 132 participants with stable COPD and randomly allocate them into pulmonary-based Qigong exercise group, acupuncture group, pulmonary-based Qigong exercise and acupuncture combined group, or control group at a 1:1:1:1 ratio. All participants will receive usual medical care and health education; those in the intervention groups will receive PQ exercise, acupuncture treatment, or a combination of both treatments three times per week for 8 weeks. The primary outcome will be the exercise endurance as assessed by a 6-min walk test. Secondary outcomes will include lung function, degree of dyspnea, diaphragmatic function, respiratory muscle strength, skeletal muscle structure, skeletal muscle function, psychological states, and quality of life. Exploratory outcomes will include the levels of inflammatory mediators. The frequency and severity of acute exacerbations of COPD will be recorded at baseline and 1 year after intervention. Discussion The findings of this study will clarify the effects of the combination of PQ exercise and acupuncture therapy on the multi-system function of patients with stable COPD to provide evidence for acupuncture as an adjuvant therapy for pulmonary rehabilitation. Clinical trial registration https://www.chictr.org.cn, ChiCTR2300076255

A core philosophy of occupational therapy is adopting a holistic approach, considering individuals' cultural and societal values. While occupational therapy is rooted in modern Western cultures, which contrasts with traditional Chinese medicine (TCM) health beliefs, TCM conceptualizes health as multidimensional-a notion akin to occupational therapy's philosophy. This article attempts to explore the relationships between TCM health culture and occupational therapy perspectives by integrating culturally relevant activities and traditional Chinese Wellness practices into clinical occupational therapy. Using the Occupational Therapy Practice Framework, the study aims to develop a reference that recommends culturally relevant activities and integrates TCM health culture into clinical occupational therapy.

Chronic exposure to environmental hazards causes airway epithelial dysfunction, primarily impaired physical barriers, immune dysfunction, and repair or regeneration. Impairment of airway epithelial function subsequently leads to exaggerated airway inflammation and remodeling, the main features of chronic obstructive pulmonary disease (COPD). Mitochondrial damage has been identified as one of the mechanisms of airway abnormalities in COPD, which is closely related to airway inflammation and airflow limitation. In this review, we evaluate updated evidence for airway epithelial mitochondrial damage in COPD and focus on the role of mitochondrial damage in airway epithelial dysfunction. In addition, the possible mechanism of airway epithelial dysfunction mediated by mitochondrial damage is discussed in detail, and recent strategies related to airway epithelial-targeted mitochondrial therapy are summarized. Results have shown that dysregulation of mitochondrial quality and oxidative stress may lead to airway epithelial dysfunction in COPD. This may result from mitochondrial damage as a central organelle mediating abnormalities in cellular metabolism. Mitochondrial damage mediates procellular senescence effects due to mitochondrial reactive oxygen species, which effectively exacerbate different types of programmed cell death, participate in lipid metabolism abnormalities, and ultimately promote airway epithelial dysfunction and trigger COPD airway abnormalities. These can be prevented by targeting mitochondrial damage factors and mitochondrial transfer. Thus, because mitochondrial damage is involved in COPD progression as a central factor of homeostatic imbalance in airway epithelial cells, it may be a novel target for therapeutic intervention to restore airway epithelial integrity and function in COPD.

Chronic obstructive pulmonary disease (COPD) is a common disease that seriously jeopardizes human health and affects patients' quality of life. The clinical efficacy of acupuncture in treating COPD is definite, and it can exert positive effects such as improving skeletal muscle degradation, airway mucus hypersecretion and pulmonary vascular remodeling in COPD rats. In recent years, the research on the underlying mechanisms of acupuncture in improving COPD has become more and more in-depth. In this review, we searched and organized the domestic and international literatures on the basic experimental aspects of acupuncture in COPD treatment, and found that the underlying mechanisms of acupuncture mainly include (1) reducing the number of inflammatory cells in the lung tissue, regulating inflammasome, epigenetic modification and inflammation-related signaling pathways to inhibit the synthesis and release of cytokines, inhibiting the level of autophagy and inhibiting the release and expression of neurotransmitters； (2) improving antioxidant capacity and reducing oxidative damage, suppressing oxidative stress in the lung tissue； (3) regulating protease/antiprotease imbalance to maintain pulmonary homeostasis. These results provide a theoretical basis and a new way of thinking for the clinical application of acupuncture in the treatment of COPD.