BackgroundThis study aimed to investigate the role of myofiber-specific TGF-β signaling in the development of muscle inflammation by modulating Treg-cell-mediated macrophage efferocytosis.MethodsCTX-induced muscle injury was performed in the tibialis anterior (TA) of control (TGF-βr2flox/flox) and transgenic mice with skeletal muscle-specific deletion of TGF-β receptor 2 (SM TGF-βr2−/−). Gene levels of regulatory T cell (Treg) activation markers and inflammatory mediators produced by macrophages or Tregs were assessed using qRT-PCR. Intramuscular infiltration of Tregs and macrophages, as well macrophage phenotypes, efferocytic function, and associated signaling molecules, were evaluated using hematoxylin and eosin (HE) staining, immunofluorescence, immunoblotting and FACS analysis. The correlation of myofibers with Tregs-mediated macrophage efferocytosis were addressed under an in vitro co-culture system, which including Tregs, macrophages, and the differentiated myogenic precursor cells (MPC-myotubes) isolated from control or SM TGF-βr2−/−mice. Apoptotic cells were generated by UV irradiation prior to transfer into inflamed muscle.ResultsDeficiency in muscle TGF-β signaling resulted in more severe muscle inflammation, characterized by an increased number of M1 macrophages and a decreased number of M2 macrophages. Notably, the absence of muscle TGF-β signaling impaired the efferocytic capacity of macrophages and reduced the proportion of Tregs in inflamed muscle. Further, we monitored that activation of intrinsic TGF-β signaling suppresses myofiber IL-6 production, which in turn impacted on IL-13 production from Tregs accumulated in damaged muscle. This ultimately facilitates IL-10-STAT3-Vav1-mediated macrophage efferocytosis in inflamed muscle.ConclusionsOur findings establish a link between muscle-specific TGF-β signaling, myokine IL-6, Tregs derived IL-13 and macrophage efferocytosis in inflamed muscle. These results suggest that therapeutic targeting of this axis may hold promise for promoting muscle regeneration.

OBJECTIVE:To develop electrospun polycaprolactone/gelatin (P/G) nanofibers modified with epigallocatechin gallate‑selenium nanoparticles (EGCG@Se) and evaluate their osteogenic effects in vitro and in vivo. METHODS:P/G nanofibers were fabricated by electrospinning, and EGCG@Se nanoparticles were synthesized using cysteine as a reducing agent. Composite fibers were formed by surface deposition and characterized using SEM, WCA, EDS, FTIR, AFM, and mechanical tests. In vitro, MSCs and MC3T3-E1 cells were cultured on P/G-EGCG@Se fibers under osteogenic induction. A tibial defect model in KM mice was used for in vivo osteogenic evaluation. Gene and protein expression were analyzed by qPCR, Western blot and ELISA. RESULTS:P/G fibers with an 8:2 weight ratio and 12 kV voltage exhibited optimal properties. EGCG@Se enhanced MSCs viability, adhesion and osteogenic differentiation. In vitro, 7.5 μg/mL Se-loaded fibers showed the best osteoinductive effect. However in vivo, 15 μg/mL Se-loaded fibers resulted in the optimal tibial defect repair, which significantly suppressed IL-6 expression in skeletal muscle. In vitro co-culturing test demonstrated that Se content in P/G-EGCG@Se nanofibers controls IL-6 production in muscle fibers. CONCLUSIONS:The special physicochemical properties of P/G-EGCG@Se fibers, assisted by bone repair effects of EGCG, and by the optimal Se content induced IL-6 level reduction from muscle tissue, contribute to the efficient bone defect healing in vivo.

Asthma exhibits pronounced circadian variation, yet the molecular mechanisms linking clock disruption to airway epithelial injury remain unclear. In this study, we identify the core clock component BMAL1 as a critical epithelial regulator that restrains ferroptosis-associated injury during allergic airway inflammation. Using a house dust mite (HDM)-induced murine asthma model and HDM-stimulated human bronchial epithelial cells, we found that BMAL1 expression was significantly reduced, whereas BMAL1 deficiency markedly aggravated airway inflammation, mucus metaplasia, and remodeling. Integrated transcriptomic and metabolomic analyses revealed a signature of inflammatory activation and metabolic reprogramming linked to ferroptosis. Consistently, BMAL1 deficiency increased lipid peroxidation and reactive oxygen species levels, downregulated GPX4 and xCT (SLC7A11), and upregulated COX2 expression in the airway epithelium both in vivo and in vitro. Treatment with Ferrostatin-1 attenuated these alterations and partially rescued the aggravated asthmatic phenotype in Bmal1-deficient mice. Notably, constitutive overexpression of BMAL1 also worsened HDM-induced airway pathology, suggesting that disruption of BMAL1 rhythmic oscillation contributes to disease progression. Mechanistically, BMAL1 deficiency activated the AP-1 pathway, induced COX2 expression, and promoted ferroptosis-associated epithelial injury, whereas inhibition of JUN alleviated this phenotype. Furthermore, melatonin also mitigated the aggravated airway pathology and ferroptosis-related changes associated with BMAL1 deficiency. Collectively, these findings identify BMAL1 as a key regulator of airway epithelial ferroptosis and highlight JUN signaling, together with COX2-associated prostaglandin responses, as downstream components of asthma exacerbations driven by circadian dysregulation.

With the growing interest in skeletal muscle diseases, understanding the processes, factors, and treatments associated with muscle regeneration is crucial. Skeletal muscle regeneration is a complex process that largely depends on the niche composed of cell populations, such as satellite cells, and their microenvironment. Cellular senescence is associated with various physiological processes and age-related diseases and plays a significant role in the muscle regeneration niche. Deciphering senescence-associated alterations within this niche provides critical insights for developing targeted anti-aging therapies. This review synthesizes recent studies to elucidate the composition of the niche and its cell-cell interactions and outlines the effects of aging on muscle regeneration and corresponding therapeutic strategies. This review summarizes emerging findings and technologies in muscle regeneration, analyzing therapeutic potential and limitations of current approaches for age-related conditions to support research advancement.

Asthma is a chronic respiratory disease with increasing global prevalence, often linked to disrupted airway microbiota. Azithromycin has shown promise in asthma treatment, but whether its effect is owing to its antimicrobial capacity remains largely unknown. A house dust mite (HDM)-induced asthmatic mouse model was used to evaluate the effects of azithromycin on airway inflammation and microbiota. Mice were divided into control, HDM-induced asthma, HDM + azithromycin, and azithromycin-alone groups. Airway microbiota was analyzed using 16S rRNA sequencing, and metabolomic profiles were assessed via liquid chromatography-tandem mass spectrometry. Azithromycin alleviated type 2 airway inflammation in HDM-induced asthma, restoring microbiota diversity by modulating specific genera, including Streptococcus, Staphylococcus, Ruminococcus, Coprococcus, Bifidobacterium, etc. Combination analysis with metabolomics revealed that azithromycin significantly regulated airway microbiota-associated sphingomyelin metabolism. Azithromycin's therapeutic effects in asthma are associated with its ability to regulate airway microbiota and its associated sphingomyelin metabolism, highlighting the potential for microbiota-targeted therapies in asthma.IMPORTANCEAsthma, a prevalent chronic respiratory condition, poses a significant global health challenge due to its increasing prevalence and associated morbidity. The role of airway microbiota in asthma pathogenesis is gaining attention, with evidence suggesting that disruptions in this microbial community contribute to disease severity. Our study investigates the impact of azithromycin, a macrolide antibiotic, on airway inflammation and microbiota in a mouse model of asthma. The findings reveal that azithromycin not only alleviates airway inflammation but also restores microbiota diversity and modulates microbiota-associated sphingomyelin metabolism. This research underscores the potential of microbiota-targeted therapies in asthma management, offering a novel therapeutic strategy that could improve patient outcomes and reduce the healthcare burden associated with asthma.

To enhance the biocompatibility and drug delivery efficiency of graphene oxide (GO), poly(ethylene glycol) (PEG), poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV), or its triblock copolymer PEG-PHBV-PEG (PPP) were used to chemically modify GO. However, it is still unknown whether non-toxic polymer-modified GO mediates muscle toxicity or triggers intramuscular inflammation. This study aims to investigate the biological reactivity and inflammation/immune response induced by PEG, PHBV, or PPP modified GO when injected into the tibialis anterior (TA) muscle of mice prior to drug loading. The results showed that after muscle exposure, the coating of biocompatible polymers on GO is more likely to provoke muscle necrosis. Muscle regeneration was found to occur earlier and more effectively in muscle treated with hydrophilic PEG-GO and PPP-GO compared to muscle treated with hydrophobic PHBV-GO. When observing the transient muscle macrophage invasion of three modified GOs, PHBV-GO caused severe muscle necrosis in the early stage, induced a delayed peak of macrophage aggregation, and caused severe inflammatory progression. All three kinds of modified GO induced T cell aggregation to varying degrees, but PEG-GO induced early mass muscle recruitment of CD4+ T cells and was more sensitive to cytotoxic T cells. Based on the higher biocompatibility of PPP-GO in muscles, PPP-GO was implanted into the muscles of old or adult mice. Compared to adult mice, aged mice are more vulnerable to the stress from PPP-GO, as demonstrated by a delayed inflammatory response and muscle regeneration.

Lung cancer is the leading cause of cancer-related death worldwide, and patients with distant metastasis have a poor prognosis. Various studies have reported that microbiota and metabolites significantly differ between healthy individuals and lung cancer patients. However, the effects of metabolites on tumor formation and metastasis are unclear. Therefore, our study aimed to determine the correlation between airway metabolites and microbiota, along with their respective roles in lung cancer metastasis. Bronchoalveolar lavage fluid (BALF) samples were collected from 30 non-small cell lung cancer (NSCLC) patients, including 11 patients without metastasis (M0) and 19 patients with metastasis (M1). Integrated pathogenic metagenomic and Liquid chromatography-mass spectrometry (LC‒MS) analyses were employed to explore differences between two groups. The omics data were analyzed and integrated via Spearman’s correlation coefficient. Specific metabolites were subsequently used to intervene in lung cancer cells and animal models to assess their influence on tumor metastasis. A total of 801 metabolites were identified in the BALF of all patients. Compared with those in the M0 group, 48 metabolites in the M1 group were significantly different. D-phenylalanine was notably upregulated in M1 and was positively related to Metamycoplasma salivarium. Intranasal administration of D-phenylalanine promoted tumor intrapulmonary metastasis and induced epithelial mesenchymal transition (EMT) process in NSCLC mouse models. Moreover, D-phenylalanine promotes the proliferation of non-small cell lung cancer cells and facilitates their migration and invasion via EMT. The airway microbiota associated D-phenylalanine could promote lung cancer metastasis via EMT, which could be a new predictor for the diagnosis of tumor metastasis in NSCLC patients.

Circadian rhythm disruption has been increasingly implicated in asthma and glucocorticoid (GC) resistance. In this study, we discovered that disruption of the brain and muscle ARNT-like 1 (BMAL1), a significant activator of the circadian clock transcription, not only exacerbated allergic inflammation but also induced GC resistance. The absence of BMAL1 intensified airway inflammation by activating the NF-κB and AP-1 pathways and also impaired the anti-inflammatory effect of GC. Our findings indicated that the deletion of BMAL1 reduced the phosphorylation level of the GC receptor (GR-Ser211), which has a direct effect on the efficacy of GC and serves as a key indicator of GR activation. Additionally, BMAL1 has a negative regulatory effect on the phosphatase dual specificity protein phosphatase 4 (DUSP4) of p38 mitogen-activated protein kinase (p38MAPK), which plays a crucial role in the phosphorylation of GR. Consequently, our findings suggest that the absence of BMAL1 results in the resistance of airway epithelial cells to GC due to the inhibition of GR phosphorylation via the DUSP4-p38MAPK axis in HDM-induced asthma. We demonstrated that the inhibition of DUSP4 restored GR activation and improved GC responsiveness, highlighting a potential therapeutic strategy for GC resistance driven by circadian disruption. Regulating the sleep disorder and circadian rhythm of patients with asthma could become a potential treatment to increase GC sensitivity.

ABSTRACTObjectivesTreating femoral neck fractures remains a significant challenge for orthopedic surgeons and imposes a substantial economic burden on developing regions. Current novel internal fixation methods demonstrate excellent biomechanical performance. However, these new internal fixation methods are still associated with various complications. This study aimed to report the clinical complications of femoral neck system (FNS) and biplane double‐supported screw fixation (BDSF) treatments for femoral neck fractures at our institution and provide directions for selecting cost‐effective internal fixation methods.MethodsA retrospective case–control study of adult patients with femoral neck fractures treated with BDSF or FNS was conducted at Nanfang Hospital from April 2019 to April 2022. General medical records were collected both preoperatively and intraoperatively. Primary complication measures included osteonecrosis of the femoral head, nonunion, screw‐out, and subtrochanteric fractures, along with femoral neck shortening. The primary functional measure evaluated was the Harris hip score. This study employed t‐test, Wilcoxon rank‐sum test, and chi‐square test to statistically analyze the data.ResultsStatistically significant differences were observed between the BDSF and FNS groups in terms of surgery duration (60.8 ± 12.6 min vs. 71.0 ± 12.0 min), incision length (5.5 ± 1.2 cm vs. 9.1 ± 1.6 cm) and hospitalization costs (39563.8 ± 9086.4 RMB vs. 24960.4 ± 10154.4 RMB). No statistically significant differences between the BDSF and FNS groups were found in the baseline data, blood loss or hospital stay. Moderate femoral neck shortening was significantly less common in the BDSF group than in the FNS group (27.1% vs. 61.5%, p = 0.016). Postoperatively, no statistically significant differences in complication rates, such as femoral head necrosis, nonunion, subtrochanteric fractures or screw‐out, were observed between the BDSF and FNS groups.ConclusionsThis study revealed no significant difference in the incidence of postoperative complications such as femoral head necrosis, nonunion or screw cut‐out between BDSF and FNS. Although BDSF has drawbacks, such as a long learning curve and the potential to cause subtrochanteric fractures, it is cost‐effective and better maintains the length of the femoral neck. The modified BDSF technique may be more suitable for developing regions with limited health care budgets.

Backgroud:Reduction of valgus-impacted femoral neck fractures remains a major challenge for orthopedic surgeons. Most reduction techniques require extensive surgical experience, and intraoperative reduction evaluation standards do not exist. The aim of this study is to report the use of a noninvasive extracapsular traction reduction technique for valgus-impacted femoral neck fractures and our innovative use of a smartphone application to evaluate reduction outcomes. Methods:We conducted a retrospective study on patients with valgus-impacted femoral neck fractures who underwent the noninvasive extracapsular traction reduction technique at a hospital between December 2022 and January 2024. General medical records from the preoperative, intraoperative, and postoperative periods were collected, with particular emphasis on evaluating intraoperative reduction effectiveness. The primary reduction indicator was the reduction angle (RA). The principal functional assessment indicator was the Harris Hip Score (HHS). Results:Radiographic measurements demonstrated significant differences between preoperative and postoperative RAs on the affected side (p < 0.05), while no differences in the RAs were observed between the unaffected side and postoperative affected side (p > 0.05). No statistically significant difference was detected between the intraoperative and postoperative radiographic measurements of the RAs on the affected side (p > 0.05). The follow-up period ranged from 12 to 25 months, with a mean duration of 17.7 ± 3.5 months. Preoperative HHS averaged 37.9 ± 5.2 points, increasing to 88.7 ± 4.1 points at final follow-up. Both 6-month and 1-year postoperative HHS showed significant improvement compared to preoperative values (p < 0.05). No fixation failure was observed during the follow-up, with a radiographic failure rate of 0% at final assessment. Conclusions:For valgus-impacted femoral neck fractures, the bone hook-assisted noninvasive extracapsular traction reduction technique can achieve optimal reduction without causing intraarticular cartilage damage. The RA helps evaluate the quality of intraoperative reduction. ImageMeter can be an effective tool for evaluating fracture reduction intraoperatively.

Asthma is a major chronic non-communicable respiratory disease, affecting over 300 million individuals globally, with an adult prevalence of 4.3

The descending genicular artery (DGA) and medial thigh region have been underused as donor sites for perforator flaps. This study evaluated the anatomical relationship between the perforators of the DGA and the saphenous vein (SV) to review the clinical applications of the free descending genicular artery perforator (DGAP) flap for locoregional reconstruction. Fifteen cadavers were arterially perfused with red latex and dissected. Thirty-one patients with extremity tissue defects were treated with a free DGAP flap, including six patients who received a chimeric flap. The minimum distance between the DGAP and the SV was measured during surgery. In all patients, the skin branch of the descending genicular artery was found in the medial femoral condyle plane in front of the SV. The average distance between the descending genicular artery perforator and the SV was 3.71 ± 0.38 cm (range: 2.9–4.3 cm). Thirty flaps survived completely, and one flap developed partial necrosis; however, this flap healed two weeks after skin grafting. The average follow-up time was 11.23 months. We conclude that the SV can be preserved when harvesting the descending genicular artery perforator flap, causing less damage to the donor site and having no effect on flap survival. The free descending genicular artery perforator flap without the SV is a better therapy for complicated tissue defects.

ABSTRACTDespite recent advances in treatment, non–small cell lung cancer (NSCLC) continues to have a high mortality rate. Currently, NSCLC pathogenesis requires further investigation, and therapeutic drugs are still under development. Homologous recombination repair (HRR) repairs severe DNA double‐strand breaks. Homologous recombination repair deficiency (HRD) occurs when HRR is impaired and causes irreparable double‐strand DNA damage, leading to genomic instability and increasing the risk of cancer development. Poly(ADP‐ribose) polymerase (PARP) inhibitors can effectively treat HRD‐positive tumors. Extracellular heat shock protein 90α (eHSP90α) is highly expressed in hypoxic environments and inhibits apoptosis, thereby increasing cellular tolerance. Here, we investigated the relationship between eHSP90α and HRR in NSCLC. DNA damage models were established in NSCLC cell lines (A549 and H1299). The activation of DNA damage and HRR markers, apoptosis, proliferation, and migration were investigated. In vivo tumor models were established using BALB/c nude mice and A549 cells. We found that human recombinant HSP90α stimulation further activated HRR and reduced DNA damage extent; however, eHSP90α monoclonal antibody, 1G6‐D7, effectively inhibited HRR. HRR inhibition and increased apoptosis were observed after LRP1 knockdown; this effect could not be reversed with hrHSP90α addition. The combined use of 1G6‐D7 and olaparib caused significant apoptosis and HRR inhibition in vitro and demonstrated promising anti‐tumor effects in vivo. Extracellular HSP90α may be involved in HRR in NSCLC through LRP1. The combined use of 1G6‐D7 and PARP inhibitors may exert anti‐tumor effects by inhibiting DNA repair and further inducing apoptosis of NSCLC cells.

Heat Shock protein 90 α (HSP90α), an main subtype of chaperone protein HSP90, involves important biological functions such as DNA damage repair, protein modification, innate immunity. However, the potential role of HSP90α in asthma occurrence and development is still unclear. This study aimed to elucidate the underlying mechanism of HSP90α in asthma by focusing on the cGAS-STING-Endoplasmic Reticulum stress pathway in inflammatory airway epithelial cell death (i.e., pyroptosis; inflammatory cell death). To accomplish that, we modeled allergen exposure in C57/6BL mice and bronchial epithelial cells with house dust mite. Protein technologies and immunofluorescence utilized to study the expression of HSP90α, activation of cGAS-STING pathway and pyroptosis. The effect of inhibitors on HDM-exposed mice detected by histological techniques and examination of bronchoalveolar lavage fluid. Results showed that HSP90α promotes asthma inflammation via pyroptosis and activation of the cGAS-STING-ER stress pathway. Treatment with the HSP90 inhibitor tanespimycin (17-AAG) significantly relieved airway inflammation and abrogated the effect of HSP90α on pyroptosis and cGAS-STING-ER stress in vitro and in vivo models of HDM. Further data indicated that up-regulation of HSP90α stabilized STING through interaction, which increased localization of STING on the ER. Activation of STING triggered ER stress and leaded to pyroptosis-related airway inflammation. The finding showed the potential role of pyroptosis caused by dysregulation of HSP90α on airway epithelial cells in allergic inflammation, suggested that targeting HSP90α in airway epithelial cells might prove to be a potential additional treatment strategy for asthma.

To explore the role of skeletal muscle specific TGF-β signaling on macrophages efferocytosis in inflamed muscle caused by Cardiotoxin (CTX) injection. CTX myoinjury was manipulated in TGF-βr2flox/flox (control) mice or transgenic mice with TGF-β receptor 2 (TGF-βr2) being specifically deleted in skeletal muscle (SM TGF-βr2−/−). Gene levels of TGF-β signal molecules, special inflammatory mediators in damaged muscle or in cultured and differentiated myogenic precursor cells (MPC-myotubes) were monitored by transcriptome microarray or qRT-PCR. TGF-β pathway molecules, myokines and embryonic myosin heavy chain in regenerating myofibers, the phenotype and efferocytosis of macrophages were evaluated by immunofluorescence, immunoblotting, Luminex, or FACS analysis. In vitro apoptotic cells were prepared by UV-irradiation. In control mice, TGF-β-Smad2/3 signaling were significantly up-regulated in regenerating centronuclear myofibers after CTX-myoinjury. More severe muscle inflammation was caused by the deficiency of muscle TGF-β signaling, with the increased number of M1, but the decreased number of M2 macrophages. Notably, the deficiency of TGF-β signaling in myofibers dramatically affected on the ability of macrophages to conduct efferocytosis, marked by the decreased number of Annexin-V−F4/80+Tunel+ macrophages in inflamed muscle, and the impaired uptake of macrophages to PKH67+ apoptotic cells transferred into damaged muscle. Further, our study suggested that, the intrinsic TGF-β signaling directed IL-10-Vav1-Rac1 efferocytosis signaling in muscle macrophages. Our data demonstrate that muscle inflammation can be suppressed potentially by activating the intrinsic TGF-β signaling in myofibers to promote IL-10 dependent-macrophages efferocytosis.

Background Minimally invasive reduction and fixation of intra‐articular calcaneal fractures poses great challenges for orthopaedic surgeons. The aim of the present study was to report the technical points, evaluate the efficacy of minimally invasive reduction and internal fixation assisted by the temporary limb reconstruction system (LRS) external fixator for intra‐articular calcaneal fractures, and propose the indications of our protocol. Methods In this retrospective study, a series of 34 consecutive closed and displaced intra‐articular calcaneal fractures involving the articular surface were treated by this technology between June 2016 and April 2018. X‐ray and computed tomography (CT) scans were performed before and after surgery to measure Bohler's angle; the length, height, and width of the calcaneus; and the mechanical axis of the hindfoot. Postoperative complications were recorded. Imaging and clinical outcomes were comprehensively evaluated using the American Orthopaedic Foot and Ankle Society (AOFAS) hindfoot‐ankle scoring system. After testing the normality of the data, Bohler's angle and the length of calcaneus were compared using the Wilcoxon signed‐rank test. The height, width of the calcaneus, and the mechanical axis of the hindfoot were compared using the Paired‐Samples t‐test. Results Thirty‐two fractures were followed up for an average of 20.66 months (from 12 to 32 months). All fractures achieved stable reduction and bony union. The articular surface was reduced and fixed with direct vision through the sinus tarsi incision. No failure of internal fixation or loss of reduction was detected during follow‐up. There were no soft tissue complications. Bohler's angle; the length, height, and width of the calcaneus; and the mechanical axis of the hindfoot improved significantly. The AOFAS scores averaged 84.12 points; seven cases were rated excellent, 20 good, four fair, and one poor. Conclusions For intra‐articular calcaneal fractures, minimally invasive surgery assisted with temporary LRS external fixation can reconstruct the calcaneal shape and the sub‐talar articular surface. This simple surgical modality with limited complications may be helpful in the surgical treatment of most type II and III calcaneal fractures except comminuted fractures of the calcaneal tuberosity.

目的 探究骨骼肌内源TGF-β信号对肌毒素诱导的小鼠急性损伤肌内巨噬细胞胞葬的影响.方法 选择野生C57BL/6鼠(对照)、肌纤维条件性TGF-β受体II敲除鼠(SMTGF-βr2-/-).Cardiotoxin(CTX)胫骨前肌(TA)注射诱导小鼠急性肌损伤.比较两组动物损伤肌内巨噬细胞渗出及表型、凋亡细胞数目、巨噬细胞胞葬差异.紫外照射法体外诱导细胞凋亡.体外分化培养原代野生鼠(WT),或SMTGF-βr2-/-鼠成肌细胞(MPCs),与巨噬细胞、凋亡细胞共培养,对比分析巨噬细胞胞葬差异.结果 较之WT鼠,SMTGF-βr2-/-鼠损伤肌内炎性渗出显著,以单核/巨噬细胞为主.M1细胞比例增加(P＜0.05),但M2细胞比例、胞葬作用显著下调(P＜0.05).体外炎性环境中,TGF-βr2-/--MPCs共培养体系中的巨噬细胞胞葬、M2巨噬细胞比例较之WT-MPCs均显著下调(P＜0.05).结论 内源TGF-β信号活化肌纤维参与调控巨噬细胞表型,可促进损伤肌内巨噬细胞胞葬,有助于局部炎症舒缓,加快肌修复.