Although ginseng marc has been routinely discarded as a waste, it still contains considerable amounts of bioactive compounds, including polysaccharides. This study assessed the protective effects of a low-molecular-weight neutral glucan, SN-GOS, obtained by enzymatic degradation of polysaccharides from Panax ginseng marc, against ulcerative colitis (UC) using human intestinal HT-29 cells and dextran sulphate sodium (DSS)-induced inflammatory colitis mice models. Correlation NMR spectroscopy and methylation analysis confirmed that SN-GOS is a starch-like branched glucan consisting mainly of glucose (92.67 mol%) and having a backbone composed of (1 → 4)(1 → 6)-α-d-glucopyranosyl units, with other minor sugars and variable linkages. SN-GOS (25-500 μg/mL) significantly suppressed TNF-α-induced inflammatory apoptotic death of HT-29 cells by downregulating caspase-9 cleavage, DNA fragmentation, disruption of mitochondrial membrane potential (MMP), and upregulating Bcl-2 expression. SN-GOS also attenuated pro-inflammatory cytokine expression (TNF-α and interleukin-6) and ROS generation caused by TNF-α treatment. In addition, SN-GOS increased LC3-II expression with a concomitant reduction in p62/SQSTM1 accumulation, suggesting activation of autophagy-associated responses. Furthermore, SN-GOS attenuated TNF-α-induced phosphorylation of ERK and p38 MAPK, suggesting modulation of inflammatory stress-related MAPK signaling. Oral administration of SN-GOS (200-400 mg/kg) resulted in significant recovery of colon length, body weight, and damaged crypts and ulcerative tissues in DSS-induced colitis mice. These results suggest that SN-GOS alleviates UC-associated inflammatory injury by inhibiting inflammatory apoptotic cell death, promoting autophagy-associated responses, and suppressing inflammatory MAPK signaling, supporting its potential use as a functional food ingredient for UC management.

Firefighters across the world face higher risks of occupational hazards, such as exposure to chemicals, extreme heat, traumatic stressors, and intense physical demands, which can increase their vulnerability to a range of psychological and physiological difficulties. These challenges include the risk of developing chronic stress, depression, and post-traumatic stress disorder (PTSD), potentially leading to detrimental negative coping patterns such as alcohol abuse. The consequent health implications impact both short-term and long-term health and well-being. This study aimed to explore the relationship between mental health status, alcohol consumption patterns, and gut microbiome alterations in firefighters from two different regions—America and Korea. By investigating these relationships, we hope to gain insights into how repeated exposure to severe stressors impacts gut health. Healthy male firefighters (ages 21–50) and controls (matched sex, geography, and age) were recruited via flyers and snowball sampling in the United States and South Korea, resulting in 203 participants (102 firefighters and 101 controls). Firefighters reported significantly higher PTSD symptoms and depression and drank 2.3 times more alcohol than the control group. American firefighters reported more drinking than Koreans. There was a significant correlation between higher alcohol consumption and the likelihood of witnessing deaths by suicide. However, there were no correlations between alcohol consumption and PTSD symptom severity. There were associations between alcohol consumption patterns and aspects of the gut microbiome. This study highlights the mental health challenges faced by firefighters, including elevated rates of PTSD, depression, and alcohol consumption, with specific microbial imbalances linked to PTSD and alcohol use, emphasizing the role of the gut–brain axis.

Recent therapeutic advances in breast cancer (BC) have improved survival outcomes; however, the prognosis for patients with bone metastasis (BM) remains poor. Hence, novel clinical biomarkers are needed to accurately predict BC BM as well as to promote personalized medicine. Here, we discovered a novel biomarker, TOR1B, for BM in BC patients via analysis of BC gene expression data and clinical information downloaded from open public databases. In cancer cells, we found high expression levels of TOR1B in the nucleus and endoplasmic reticulum. Regarding gene expression, the level of TOR1B was significantly upregulated in BC patients with BM ( p < 0.05), and the result was externally validated. In addition, gene expression clearly demonstrated two distinct types of prognoses in ER- and PR-positive patients. In multivariate regression, the gene could be an independent predictor of BM in BC patients, i.e., a low expression level of TOR1B was associated with delayed metastasis to bone in BC patients (HR, 0.28; 95% CI 0.094–0.84). Conclusively, TOR1B might be a useful biomarker for predicting BM; specifically, patients with ER- and PR-positive subtypes would benefit from the clinical use of this promising prognostic biomarker.

Turner syndrome (TS), a genetic disorder due to incomplete dosage compensation of X-linked genes, affects multiple organ systems, leading to hypogonadotropic hypogonadism, short stature, cardiovascular and vascular abnormalities, liver disease, renal abnormalities, brain abnormalities, and skeletal problems. Patients with TS experience premature ovarian failure with a rapid decline in ovarian function caused by germ cell depletion, and pregnancies carry a high risk of adverse maternal and fetal outcomes. Aortic abnormalities, heart defects, obesity, hypertension, and liver abnormalities, such as steatosis, steatohepatitis, biliary involvement, liver cirrhosis, and nodular regenerative hyperplasia, are commonly observed in patients with TS. The SHOX gene plays a crucial role in short stature and abnormal skeletal phenotype in patients with TS. Abnormal structure formation of the ureter and kidney is also common in patients with TS, and a non-mosaic 45,X karyotype is significantly associated with horseshoe kidneys. TS also affects brain structure and function. In this review, we explore various phenotypic and disease manifestations of TS in different organs, including the reproductive system, cardiovascular system, liver, kidneys, brain, and skeletal system.

Schizophrenia, a severe mental illness affecting about 1% of the population, manifests during young adulthood, leading to abnormal mental function and behavior. Its multifactorial etiology involves genetic factors, experiences of adversity, infection, and gene–environment interactions. Emerging research indicates that maternal infection or stress during pregnancy may also increase schizophrenia risk in offspring. Recent research on the gut–brain axis highlights the gut microbiome’s potential influence on central nervous system (CNS) function and mental health, including schizophrenia. The gut microbiota, located in the digestive system, has a significant role to play in human physiology, affecting immune system development, vitamin synthesis, and protection against pathogenic bacteria. Disruptions to the gut microbiota, caused by diet, medication use, environmental pollutants, and stress, may lead to imbalances with far-reaching effects on CNS function and mental health. Of interest are short-chain fatty acids (SCFAs), metabolic byproducts produced by gut microbes during fermentation. SCFAs can cross the blood–brain barrier, influencing CNS activity, including microglia and cytokine modulation. The dysregulation of neurotransmitters produced by gut microbes may contribute to CNS disorders, including schizophrenia. This review explores the potential relationship between SCFAs, the gut microbiome, and schizophrenia. Our aim is to deepen the understanding of the gut–brain axis in schizophrenia and to elucidate its implications for future research and therapeutic approaches.

Non-alcoholic fatty liver disease (NAFLD) is a prevalent condition characterized by lipid accumulation in hepatocytes with low alcohol consumption. The development of sterile inflammation, which occurs in response to a range of cellular stressors or injuries, has been identified as a major contributor to the pathogenesis of NAFLD. Recent studies of the pathogenesis of NAFLD reported the newly developed roles of damage-associated molecular patterns (DAMPs). These molecules activate pattern recognition receptors (PRRs), which are placed in the infiltrated neutrophils, dendritic cells, monocytes, or Kupffer cells. DAMPs cause the activation of PRRs, which triggers a number of immunological responses, including the generation of cytokines that promote inflammation and the localization of immune cells to the site of the damage. This review provides a comprehensive overview of the impact of DAMPs and PRRs on the development of NAFLD.

The gut microbiome is a diverse bacterial community in the human gastrointestinal tract that plays important roles in a variety of biological processes. Short-chain fatty acids (SCFA) are produced through fermentation of dietary fiber. Certain microbes in the gut are responsible for producing SCFAs such as acetate, propionate and butyrate. An imbalance in gut microbiome diversity can lead to metabolic disorders and inflammation-related diseases. Changes in SCFA levels and associated microbiota were observed in IBD, suggesting an association between SCFAs and disease. The gut microbiota and SCFAs affect reactive oxygen species (ROS) associated with IBD. Gut microbes and SCFAs are closely related to IBD, and it is important to study them further.

Mesenchymal stem cells (MSCs) are promising candidates for tissue regeneration, cell therapy, and cultured meat research owing to their ability to differentiate into various lineages including adipocytes, chondrocytes, and osteocytes. As MSCs display different characteristics depending on the tissue of origin, the appropriate cells need to be selected according to the purpose of the research. However, little is known of the unique properties of MSCs in pigs. In this study, we compared two types of porcine mesenchymal stem cells (MSCs) isolated from the dorsal subcutaneous adipose tissue (adipose-derived stem cells (ADSCs)) and Wharton’s jelly of the umbilical cord (Wharton’s jelly-derived mesenchymal stem cells (WJ-MSCs)) of 1-day-old piglets. The ADSCs displayed a higher proliferation rate and more efficient differentiation potential into adipogenic and chondrogenic lineages than that of WJ-MSCs; conversely, WJ-MSCs showed superior differentiation capacity towards osteogenic lineages. In early passages, ADSCs displayed higher proliferation rates and mitochondrial energy metabolism (measured based on the oxygen consumption rate) compared with that of WJ-MSCs, although these distinctions diminished in late passages. This study broadens our understanding of porcine MSCs and provides insights into their potential applications in animal clinics and cultured meat science.

Background and Aims: Breast cancer (BC) is the leading cause of mortality among all cancers in Bangladeshi women. The prognosis of metastatic breast cancer depends on certain factors, like surgery, radiotherapy, chemotherapy, hormonal receptor content of the tumor or associated illness such as diabetes mellitus and obesity. Among the associated illness, diabetes mellitus is one of the most common metabolic disease worldwide, which is linked to an increased risk of developing breast cancer and an even higher risk of recurrence and dying from this disease. In this context, we studied diabetic and metabolic disease related growth and metabolic factors in breast cancer patients for assessing the prognosis of BC. Methods: A total of 180 mastectomy patients were purposively taken in the present study. Data were collected from retrospective information. Anthropometric and biochemical parameters were taken by standard methods. Growth and metabolic factors were determined by enzyme-linked immunosorbent assay (ELISA) method. Association of diabetes treatment modalities with breast cancer metastasis was evaluated by correlation analysis among 80 diabetic patients. Results: Serum level of insulin-like growth factor 1 (IGF1) was found to be significantly higher (p=0.001) in ER and PR negative breast cancer than their positive counterparts. Patients who had lymph node positive and Her2 borderline showed a significant reduction in serum adiponectin level (p<0.05) and this association was retained after adjusting the confounding variables. Furthermore, delayed treatment, IGF-1, ALP, sleeping hours were significant predictors for metastasis of breast cancer patients in Bangladesh. The Diabetic BC patients treated with both insulin and oral drug was found to be negatively associated with breast cancer metastasis compared to Diabetic-BC patients treated with only oral drugs (p<0.05). However, BC metastasis did not any have an association with serum fasting insulin or insulin resistance. Obesity also did not show any relation with BC prognosis. Conclusions: Serum IGF-1 and adiponectin may have an association with invasiveness and metastasis of breast cancer. Diabetes treatment with combination therapy ameliorates breast cancer metastasis.Breast cancer prognosis would be independently predict by serum levels of IGF-1 as well as IGF1 could be used as a screening biomarker when validated in a larger sample size. Citation Format: Salima Akter, Muhammad Saiedullah, Mousumi Bhowmik, Hajara Akhter, Shahina Ansary, Waheed Akhtar, Sufi Hannan Zulfiqur Rahman, Tae Gyu Choi, Sung Soo Kim. Predicting the metastatic potential in breast cancer patients in Bangladesh [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2099.

Background and aims: Aberrant insulin-like growth factor (IGFs) signaling is directly implicated in oncogenesis and metastasis in various solid tumors including breast cancer. Targeting the IGF axis may provide an insight into the mechanism of cancer stemness and therapy resistance. The present study aims to explore the association of the circulatory levels of these proteins in aggressive triple-negative breast cancer (TNBC) in Bangladesh. Methods: A total of 165 BC patients were recruited in the present study where 42 were TNBC subjects (selected based on their complete hormonal profile). Data were collected from retrospective information. Anthropometric and biochemical parameters were measured by standard methods. Serum IGF1, IGFBP1, and insulin were estimated by ELISA. Results: TNBC subjects showed significantly higher levels of circulatory IGF1 (185 vs 145, p=0.004), while patients who had distant metastasis showed increased levels of IGF1, IGFBP1, and alkaline phosphatase (ALP) [178 vs 153, p=0.001; 6.44 vs 3.05, and 140 vs 88, p<0.05; metastatic vs non-metastatic BC respectively]. In addition, serum IGF1 was positively associated with serum insulin levels and IGFBP1 was associated with ALP, SGPT, CA15.3, and duration of OCP (p<0.05). In multivariate regression, IGF1 was found to be a significant predictor of breast cancer survival after adjusting confounding variables. Conclusion: High serum levels of IGF1 may contribute to metastasis in basal breast cancer in a Bangladeshi population. These results need to be confirmed in larger TNBC survivor cohorts. Citation Format: Salima Akter, Mithila Faruque, Hajara Akhter, Mousumi Bhowmik, Mohammad Nazmul Hasan, Lipika Sultana, Imran Khan, Mamun Mia, Md. Mustafizur Rahman, Habib Sadat Chaudhury, Islam S. Rafiqul, Kamrun Nahar, Tae Gyu Choi, Sung Soo Kim. Circulatory insulin-like growth factor 1 predicts metastasis in triple-negative breast cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 1526.

Particulate matters (PMs) from polluted air cause diverse pulmonary and cardiovascular diseases, including lung inflammation. While the fruits (Goji) of Lycium trees are commonly consumed as traditional medicine and functional food ingredients, the majority of their roots are discarded as by-products. To enhance the industrial applicability of Lycium roots, we prepared an ethanol extract (named GR30) of L. chinense Miller roots and evaluated its potential protective effects against particulate matter 10 (PM10)-induced inflammation and immune cell death. The GR30 treatment (0–500 μg/mL) significantly attenuated the PM10-induced cell cycle arrest, DNA fragmentation and mitochondria-dependent apoptosis in RBL-2H3 basophil cells. GR30 also significantly antagonized the PM10-induced expression of proinflammatory cytokines (IL-4, IL-13, and TNF-α) and COX2 expression through downregulation of MAPKs (ERK and JNK) signalling pathway. Oral administration of GR30 (200–400 mg/kg) to PM10 (20 mg/mL)-challenged mice significantly reduced the serum levels of IgE and the expression of TNF-α and Bax in lung tissues, which were elevated by PM10 exposure. These results revealed that the ethanolic extract (GR30) of L. chinense Miller roots exhibited anti-inflammatory and cyto-protective activity against PM10-induced inflammation and basophil cell death, and thus, it would be useful in functional food industries to ameliorate PM-mediated damage to respiratory and immune systems.

Metabolic syndrome (MetS) is a common feature in obesity, comprising a cluster of abnormalities including abdominal fat accumulation, hyperglycemia, hyperinsulinemia, dyslipidemia, and hypertension, leading to diabetes and cardiovascular diseases (CVD). Intake of carbohydrates (CHO), particularly a sugary diet that rapidly increases blood glucose, triglycerides, and blood pressure levels is the predominant determining factor of MetS. Complex CHO, on the other hand, are a stable source of energy taking a longer time to digest. In particular, resistant starch (RS) or soluble fiber is an excellent source of prebiotics, which alter the gut microbial composition, which in turn improves metabolic control. Altering maternal CHO intake during pregnancy may result in the child developing MetS. Furthermore, lifestyle factors such as physical inactivity in combination with dietary habits may synergistically influence gene expression by modulating genetic and epigenetic regulators transforming childhood obesity into adolescent metabolic disorders. This review summarizes the common pathophysiology of MetS in connection with the nature of CHO, intrauterine nutrition, genetic predisposition, lifestyle factors, and advanced treatment approaches; it also emphasizes how dietary CHO may act as a key element in the pathogenesis and future therapeutic targets of obesity and MetS.

In the liver, reactive oxygen species (ROS) are constantly released during cellular metabolic processes, and excess ROS production can cause redox stress. The redox stress is both beneficial for and harmful to the survival of cells since it modulates the cellular redox control system. The redox control system is a series of cellular responses that are responsible for maintaining a balanced oxidation-reduction status. Many cellular processes including growth, proliferation, and senescence are sensitively regulated by the redox control system. Imbalance of redox induces redox stress and damages DNA, proteins, and lipids in cells, and further contributes to the pathogenesis of severe diseases and disorders like cancer. However, the cellular redox control system also utilizes redox stress-responsive pathways and increases antioxidant enzymes to aid cell survival. Therefore, a deeper understanding of the connection between the redox control system and liver disease is likely to pave the way for the future development of new therapeutic strategies. This review will examine the redox control systems in liver with responsive regulating molecules, current knowledge of the redox control system and liver disease, and suggest potential therapeutic targets for liver diseases.

Alzheimer’s disease (AD), ranked as the seventh leading cause of death worldwide, is one of the most incidental neurodegenerative disorders. AD patients experience irreparable damages to the brain, indicated as progressive, insidious, and degenerative. Past research has discovered that the amyloid cascade hypothesis best describes the pathophysiological etiology of AD, designating amyloid-β plaques and neurofibrillary tangles as the ‘hallmarks’ of AD pathology. Furthermore, accumulating evidence show that the oxidative stress state, the imbalance between reactive oxygen species (ROS) production and antioxidation, contributes to AD development. This chapter describes the oxidative stress process in AD. It mainly tackles the correlation of metal-catalyzed ROS production with amyloid-β and how it oxidatively damages both the amyloid-β itself and the surrounding molecules, potentially leading to AD. Additionally, both the role of metal chelation therapy as a treatment for AD and its challenges will be mentioned as well. This chapter specially focuses on how metal ions imbalance induces oxidative stress and how it affects AD pathology.

One in three cancer deaths worldwide are caused by gastric and colorectal cancer malignancies. Although the incidence and fatality rates differ significantly from country to country, the rates of these cancers in East Asian nations such as South Korea and Japan have been increasing each year. Above all, the biggest danger of this disease is how challenging it is to recognize in its early stages. Moreover, most patients with these cancers do not present with any disease symptoms before receiving a definitive diagnosis. Currently, volatile organic compounds (VOCs) are being used for the early prediction of several other diseases, and research has been carried out on these applications. Exhaled VOCs from patients possess remarkable potential as novel biomarkers, and their analysis could be transformative in the prevention and early diagnosis of colon and stomach cancers. VOCs have been spotlighted in recent studies due to their ease of use. Diagnosis on the basis of patient VOC analysis takes less time than methods using gas chromatography, and results in the literature demonstrate that it is possible to determine whether a patient has certain diseases by using organic compounds in their breath as indicators. This study describes how VOCs can be used to precisely detect cancers; as more data are accumulated, the accuracy of this method will increase, and it can be applied in more fields.

The WHO's definition of health transcends the mere absence of disease, emphasizing physical, mental, and social well-being. As this perspective is being increasingly applied to the management of chronic diseases, research on gut microbiota (GM) is surging, with a focus on its potential for persistent and noninvasive dietary therapeutics. In patients with epilepsy (PWE), a chronic lack of seizure control along with often neglected psychiatric comorbidities greatly disrupt the quality of life. Evidence shows that GM-derived short chain fatty acids (SCFAs) may impact seizure susceptibility through modulating (1) excitatory/inhibitory neurotransmitters, (2) oxidative stress and neuroinflammation, and (3) psychosocial stress. These functions are also connected to shared pathologies of epilepsy and its two most common psychiatric consequences: depression and anxiety. As the enhancement of SCFA production is enabled through direct administration, as well as probiotics and prebiotics, related dietary treatments may exert antiseizure effects. This paper explores the potential roles of SCFAs in the context of seizure control and its mental comorbidities, while analyzing existing studies on the effects of pro/prebiotics on epilepsy. Based on currently available data, this study aims to interpret the role of SCFAs in epileptic treatment, extending beyond the absence of seizures to target the health of PWE.

Aggressive and recurrent gynecological cancers are associated with worse prognosis and a lack of effective therapeutic response. Ovarian cancer (OC) patients are often diagnosed in advanced stages, when drug resistance, angiogenesis, relapse, and metastasis impact survival outcomes. Currently, surgical debulking, radiotherapy, and/or chemotherapy remain the mainstream treatment modalities; however, patients suffer unwanted side effects and drug resistance in the absence of targeted therapies. Hence, it is urgent to decipher the complex disease biology and identify potential biomarkers, which could greatly contribute to making an early diagnosis or predicting the response to specific therapies. This review aims to critically discuss the current therapeutic strategies for OC, novel drug-delivery systems, and potential biomarkers in the context of genetics and molecular research. It emphasizes how the understanding of disease biology is related to the advancement of technology, enabling the exploration of novel biomarkers that may be able to provide more accurate diagnosis and prognosis, which would effectively translate into targeted therapies, ultimately improving patients’ overall survival and quality of life.

Objective: Our previous studies showed an age-related increased prevalence of nasal polyps (NP) and reduced production of S100A8/9 in elderly patients with chronic rhinosinusitis with NP (CRSwNP). In this study, we investigated an unbiased age-related gene expression profile in CRSwNP subjects and healthy controls, and further identified the differences in their tissue remodeling.Methods: Microarrays using NP and uncinate tissues from health controls (elderly, age ≥65 vs. non-elderly, age 18–49) were performed, and differentially regulated genes were analyzed. Quantitative real-time PCR (qPCR), Immunostaining, Periodic acid-Schiff (PAS), trichrome staining, Western blot, and ELISA were performed for further investigation.Results: Microarrays identified differentially expressed genes according to disease and age; 278 in NP vs. controls, 75 in non-elderly NP vs. non-elderly controls, and 32 in elderly NP vs. elderly controls. qPCR confirmed that the PLAT gene was downregulated and the SERPINB2 gene upregulated in NP vs. controls. The serous glandular cell-derived antimicrobial protein/peptide-related genes such as BPIFB3, BPIFB2, LPO, and MUC7 were remarkably reduced in NP, regardless of age. SERPINE1 gene (plasminogen activator inhibitor-1, PAI-1) expression was significantly increased in elderly NP versus elderly controls. IHC and western blot confirmed significantly decreased production of MUC7 and LPO in NP versus controls. There was a trend of age-related reduction of submucosal gland cells in normal controls. Trichrome and immunofluorescence staining demonstrated an age-related increase of collagen and fibrin deposition in NP, consistent with increased PAI-1 production.Conclusion: This study demonstrated age-related differential glandular remodeling patterns and fibrosis in NP and normal controls. PAI-1 expression was significantly increased in elderly NP versus elderly controls, suggesting PAI-1 as a potential treatment target in elderly NP.

The downregulation of reactive oxygen species (ROS) facilitates precancerous tumor development, even though increasing the level of ROS can promote metastasis. The transforming growth factor-beta (TGF-β) signaling pathway plays an anti-tumorigenic role in the initial stages of cancer development but a pro-tumorigenic role in later stages that fosters cancer metastasis. TGF-β can regulate the production of ROS unambiguously or downregulate antioxidant systems. ROS can influence TGF-β signaling by enhancing its expression and activation. Thus, TGF-β signaling and ROS might significantly coordinate cellular processes that cancer cells employ to expedite their malignancy. In cancer cells, interplay between oxidative stress and TGF-β is critical for tumorigenesis and cancer progression. Thus, both TGF-β and ROS can develop a robust relationship in cancer cells to augment their malignancy. This review focuses on the appropriate interpretation of this crosstalk between TGF-β and oxidative stress in cancer, exposing new potential approaches in cancer biology.

Autophagy is a catabolic process for unnecessary or dysfunctional cytoplasmic contents by lysosomal degradation pathways. Autophagy is implicated in various biological processes such as programmed cell death, stress responses, elimination of damaged organelles and development. The role of autophagy as a crucial mediator has been clarified and expanded in the pathological response to redox signalling. Autophagy is a major sensor of the redox signalling. Reactive oxygen species (ROS) are highly reactive molecules that are generated as by-products of cellular metabolism, principally by mitochondria. Mitochondrial ROS (mROS) are beneficial or detrimental to cells depending on their concentration and location. mROS function as redox messengers in intracellular signalling at physiologically low level, whereas excessive production of mROS causes oxidative damage to cellular constituents and thus incurs cell death. Hence, the balance of autophagy-related stress adaptation and cell death is important to comprehend redox signalling-related pathogenesis. In this review, we attempt to provide an overview the basic mechanism and function of autophagy in the context of response to oxidative stress and redox signalling in pathology.