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"Gong, Ge"
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ROS: Executioner of regulating cell death in spinal cord injury
The damage to the central nervous system and dysfunction of the body caused by spinal cord injury (SCI) are extremely severe. The pathological process of SCI is accompanied by inflammation and injury to nerve cells. Current evidence suggests that oxidative stress, resulting from an increase in the production of reactive oxygen species (ROS) and an imbalance in its clearance, plays a significant role in the secondary damage during SCI. The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is a crucial regulatory molecule for cellular redox. This review summarizes recent advancements in the regulation of ROS-Nrf2 signaling and focuses on the interaction between ROS and the regulation of different modes of neuronal cell death after SCI, such as apoptosis, autophagy, pyroptosis, and ferroptosis. Furthermore, we highlight the pathways through which materials science, including exosomes, hydrogels, and nanomaterials, can alleviate SCI by modulating ROS production and clearance. This review provides valuable insights and directions for reducing neuronal cell death and alleviating SCI through the regulation of ROS and oxidative stress.
Journal Article
أفكار حول تعميق الإصلاح
يناقش الكتاب سلسلة من الإيضاحات الهامة قدمها الرئيس الصيني والأمين العام للجنة المركزية للحزب الشيوعي الصيني، شي جين بينغ، وتدور حول أفكار الإصلاح وتوسيع الانفتاح على نحو شامل في الصين. يضم الكتاب أكثر من 70 وثيقة هامة على صورة كلمات شي جين بينغ وخطاباته وتعليقاته وتوجيهاته وينقسم الكتاب إلى 12 موضوعا خاصا تتضمن 274 قطعة من مقتطفات الأقوال، نشر بعضها لأول مرة.
Book
Mechanism of regulating macrophages/osteoclasts in attenuating wear particle-induced aseptic osteolysis
Joint replacement surgery is the most effective treatment for end-stage arthritis. Aseptic loosening caused by periprosthetic osteolysis is a common complication after joint replacement. Inflammation induced by wear particles derived from prosthetic biomaterials is a major cause of osteolysis. We emphasize that bone marrow-derived macrophages and their fusion-derived osteoclasts play a key role in this pathological process. Researchers have developed multiple intervention approaches to regulate macrophage/osteoclast activation. Aiming at wear particle-induced periprosthetic aseptic osteolysis, this review separately discusses the molecular mechanism of regulation of ROS formation and inflammatory response through intervention of macrophage/osteoclast RANKL-MAPKs-NF-κB pathway. These molecular mechanisms regulate osteoclast activation in different ways, but they are not isolated from each other. There is also a lot of crosstalk among the different mechanisms. In addition, other bone and joint diseases related to osteoclast activation are also briefly introduced. Therefore, we discuss these new findings in the context of existing work with a view to developing new strategies for wear particle-associated osteolysis based on the regulation of macrophages/osteoclasts.
Journal Article
Pyroptosis in spinal cord injury
Spinal cord injury (SCI) often brings devastating consequences to patients and their families. Pathophysiologically, the primary insult causes irreversible damage to neurons and glial cells and initiates the secondary damage cascade, further leading to inflammation, ischemia and cells death. In SCI, the release of various inflammatory mediators aggravates nerve injury. Pyroptosis is a new pro-inflammatory pattern of regulated cell death (RCD), mainly mediated by caspase-1 or caspase-11/4/5. Gasdermins family are pore-forming proteins known as the executor of pyroptosis and the gasdermin D (GSDMD) is best characterized. Pyroptosis occurs in multiple central nervous system cell types, especially plays a vital role in the development of SCI. We review here the evidence for pyroptosis in SCI, and focus on the pyroptosis of different cells and the crosstalk between them. In addition, we discuss the interaction between pyroptosis and other forms of RCD in SCI. We also summarize the therapeutic strategies for pyroptosis inhibition, so as to provide novel ideas for improving outcomes following SCI.
Journal Article
Potential therapeutic effects of IL28RA inhibition on acute myocardial infarction through phosphorylated JAK1/STAT1 signaling pathways
While current coronary intervention therapies and surgical bypass procedures are widely utilized, the treatment of acute myocardial infarction (AMI) in the elderly continues to pose significant challenges. Following AMI, the body’s immune system is activated, resulting in the release of inflammatory mediators that exacerbate myocardial damage. Interleukin 28A (IL28A) and interleukin 28B (IL28B) may play a role in immune regulation post-AMI by specifically binding to interleukin 28 receptor alpha (IL28RA). However, the precise underlying mechanisms remain incompletely understood. This study aims to investigate the levels of IL28A and IL28B following AMI, as well as the protective effects of inhibiting IL28RA expression in the context of AMI and its potential mechanisms. We analyzed serum samples from 55 patients with AMI and 41 control individuals using ELISA to evaluate the levels of IL28A and IL28B, as well as to assess their correlation with the clinical parameters of the patients. Additionally, we established a mouse model of AMI and employed intramyocardial injection of lentivirus to knock down IL28RA in the myocardium. Echocardiography was utilized to compare structural and functional changes, while HE staining was conducted to analyze the infarct area and assess changes in myocardial tissue and cell morphology. The expressions of IL28A, IL28B, IL28RA, and JAK1/STAT1 pathway-related proteins in the infarct area were compared through immunofluorescence and Western blot analysis. Finally, TUNEL staining and the BAX/Bcl2 ratio were utilized to evaluate cardiomyocyte apoptosis. The study demonstrated that serum IL28A levels in patients with AMI were significantly elevated compared to those in normal controls, whereas IL28B levels were significantly reduced. Additionally, both IL28A and IL28B levels exhibit a linear relationship with high-density lipoprotein (HDL) and body mass index (BMI). In a mouse model, cardiac function deteriorated and ventricular structural changes were observed 14 days post-myocardial infarction relative to controls. The expressions of IL28A and IL28RA were significantly upregulated in the myocardium of the infarcted area, while IL28B levels showed no significant variation. Additionally, the ratios of p-JAK1/JAK1 and p-STAT1/STAT1 were significantly increased, accompanied by a notable rise in apoptotic cells within the myocardial infarction area. Importantly, the knockdown of IL28RA expression in the infarcted region effectively mitigated these alterations. These results suggest that IL28A but not IL28B contributes to the process post-AMI and may induce cardiomyocyte apoptosis through the JAK1/STAT1 pathway in conjunction with IL28RA.
Journal Article
Correlation between the Charlson comorbidity index and skeletal muscle mass/physical performance in hospitalized older people potentially suffering from sarcopenia
Background
Sarcopenia is a decrease in skeletal muscle mass, physical performance, and muscle strength in older people. In this study, we aimed to explore the correlation between comorbidity and skeletal muscle mass and physical performance in older people.
Methods
This retrospective study included 168 subjects. Their medical history, physical function, computed tomography (CT) chest scans, and blood tests for nutrition were evaluated. The patients were divided into two groups: (1) a low muscle mass group and (2) a normal muscle mass group. Multivariate analysis of variance was used to compare multiple sets of mean vectors.
Results
Overall, 72.02% of the subjects had a low skeletal muscle index (SMI) and low gait speed. The patients with low skeletal muscle mass and physical performance were older, had more serious comorbidities, and had longer average hospitalization periods and lower albumin and hemoglobin levels. Subjects with a high Charlson comorbidity index (CCI) were more likely to be in the sarcopenic group than in the non-sarcopenic group. In addition, there was a linear correlation between the CCI and SMI (r = − 0.549,
P
< 0.05), and between the CCI and gait speed (r = − 0.614,
P
< 0.05). The area under the curve (AUC) value for low skeletal muscle mass with the CCI was 0.879.
Conclusions
We identified an independent association between comorbidity and skeletal muscle mass/physical performance by researching the correlation between the CCI and SMI/gait speed. Our results suggested that the CCI score may have important clinical diagnostic value for sarcopenia.
Journal Article
YAP/TAZ-mediated nuclear membrane rupture in promoting senescence of skeletal muscle associated with COPD
Patients with chronic obstructive pulmonary disease (COPD) often develop complications associated with sarcopenia; however, the underlying mechanisms remain unclear. Through a combination of in vitro and in vivo experiments, as well as bioinformatics analysis, our study identified YAP/TAZ as a key regulator of the aging phenotype in the skeletal muscle of COPD patients. In skeletal muscle affected by cigarette smoke-induced COPD, we observed significant reductions in YAP/TAZ levels, alongside markers indicative of skeletal muscle aging and dysfunction. Notably, overexpression of YAP/TAZ significantly improved these conditions. Our results suggest a novel mechanism whereby the maintenance of YAP/TAZ activity interacts with ACTR2 to preserve nuclear membrane integrity and reduce cytoplasmic dsDNA levels, thereby attenuating STING activation and cellular senescence. Additionally, we found that YAP is involved in the transcriptional regulation of the ACTR2 promoter region. Overall, preserving YAP/TAZ activity may help prevent skeletal muscle aging associated with COPD, representing a new strategy for intervening in COPD-related sarcopenia.
Clinical trial number
Not applicable.
Journal Article
The dual role of autophagy in periprosthetic osteolysis
Periprosthetic osteolysis (PPO) induced by wear particles is an important cause of aseptic loosening after artificial joint replacement, among which the imbalance of osteogenesis and osteoclastic processes occupies a central position. The cells involved in PPO mainly include osteoclasts (macrophages), osteoblasts, osteocytes, and fibroblasts. RANKL/RANK/OGP axis is a typical way for osteolysis. Autophagy, a mode of regulatory cell death and maintenance of cellular homeostasis, has a dual role in PPO. Although autophagy is activated in various periprosthetic cells and regulates the release of inflammatory cytokines, osteoclast activation, and osteoblast differentiation, its beneficial or detrimental role remains controversy. In particular, differences in the temporal control and intensity of autophagy may have different effects. This article focuses on the role of autophagy in PPO, and expects the regulation of autophagy to become a powerful target for clinical treatment of PPO.
Journal Article
Angiopoietin-1 Protects Spinal Cord Ischemia and Reperfusion Injury by Inhibiting Autophagy in Rats
Spinal cord ischemia and reperfusion (SCIR) injury can induce autophagy, which is involved in the survival of neurons. However, whether autophagy plays a neuroprotective or a detrimental role in SCIR injury remains controversial. Angiopoietin-1 (Ang-1), an endothelial growth factor, has been shown to have neuroprotective effects. The present study aimed to explore the neuroprotective mechanisms of Ang-1 in neuronal cells in a rat model of SCIR injury in vivo. Ang-1 protein and rapamycin were injected intrathecally. Basso Beattie Bresnahan (BBB) scoring and hematoxylin and eosin staining were used to assess the degree of SCIR injury. Proteins that reflected the level of autophagy expression, such as Beclin-1 and LC3, were evaluated by western blotting. The results indicated that SCIR injury resulted in loss in lower limb motor function. Ang-1 protein inhibited the expression of Beclin-1 and LC3, which improved the BBB score and alleviated spinal cord injury. In contrast, rapamycin, an autophagy activator, caused the opposite effect. This study provides evidence that Ang-1 plays a neuroprotective role by inhibiting of autophagy expression in SCIR injury. Overall, findings could be useful for the treatment of SCIR injury.
Journal Article