CPT1A Alleviates Senescence and Restores Osteogenic Differentiation of BM-MSC Through SOD2 Succinylation.

Bone marrow mesenchymal stem cells (BM-MSCs) have promising prospects in bone repair and regenerative medicine. However, BM-MSCs gradually lose their original pluripotency and differentiation potential after successive passages. This study aimed to reveal the mechanism underlying the phenomenon.

SIRT5 -mediated desuccinylation of UQCRC2 attenuates osteogenic differentiation of aged BM-MSCs through impairing mitochondrial homeostasis.

Background: The osteogenic differentiation potential of bone marrow mesenchymal stem cells (BM-MSCs) is critical for bone regeneration and repair. In recent years, the role of protein succinylation modification in regulating cellular metabolism has garnered increasing attention. However, its mechanism in osteogenic differentiation remains unclear.

Enhancement of Bone Repair in Diabetic Rats with Metformin-Modified Silicified Collagen Scaffolds.

Regenerating bone defects in diabetic rats presents a significant challenge due to the detrimental effects of reactive oxygen species and impaired autophagy on bone healing. To address these issues, a metformin-modified biomimetic silicified collagen scaffold is developed utilizing the principles of biomimetic silicification. In vitro and in vivo experiments demonstrated that the scaffold enhanced bone tissue regeneration within the diabetic microenvironment through the release of dual bio-factors.

Autophagy Promotes Cigarette Smoke-Initiated and Elastin-Driven Bronchitis-Like Airway Inflammation in Mice.

Cigarette smoke (CS)-induced macrophage activation and airway epithelial injury are both critical for the development of chronic obstructive pulmonary disease (COPD), while the eventual functions of autophagy in these processes remain controversial. We have recently developed a novel COPD mouse model which is based on the autoimmune response sensitized by CS and facilitated by elastin. In the current study, we therefore utilized this model to investigate the roles of autophagy in different stages of the development of bronchitis-like airway inflammation.

Cigarette smoke-initiated autoimmunity facilitates sensitisation to elastin-induced COPD-like pathologies in mice.

It is currently not understood whether cigarette smoke exposure facilitates sensitisation to self-antigens and whether ensuing auto-reactive T cells drive chronic obstructive pulmonary disease (COPD)-associated pathologies.To address this question, mice were exposed to cigarette smoke for 2 weeks. Following a 2-week period of rest, mice were challenged intratracheally with elastin for 3 days or 1 month.

Fixation versus Excision of Osteochondral Fractures after Patellar Dislocations in Adolescent Patients: A Retrospective Cohort Study.

Background: Patellar dislocation is one of the most common knee injuries in the adolescent population. It is often combined with osteochondral fracture. The purpose of this study was to compare the outcomes between fixation and excision of osteochondral fractures not involving the bearing surface in adolescent patients with patellar dislocations.

MTOR Suppresses Cigarette Smoke-Induced Epithelial Cell Death and Airway Inflammation in Chronic Obstructive Pulmonary Disease.

Airway epithelial cell death and inflammation are pathological features of chronic obstructive pulmonary disease (COPD). Mechanistic target of rapamycin (MTOR) is involved in inflammation and multiple cellular processes, e.g.

Endoplasmic reticulum chaperone GRP78 mediates cigarette smoke-induced necroptosis and injury in bronchial epithelium.

Introduction: Bronchial epithelial cell death and airway inflammation induced by cigarette smoke (CS) have been involved in the pathogenesis of COPD. GRP78, belonging to heat shock protein 70 family, has been implicated in cell death and inflammation, while little is known about its roles in COPD. Here, we demonstrate that GRP78 regulates CS-induced necroptosis and injury in bronchial epithelial cells.

Early growth response factor 1 is essential for cigarette smoke-induced MUC5AC expression in human bronchial epithelial cells.

Early growth response factor 1 (Egr-1) is a zinc finger transcription factor which responses rapidly to a variety of extracellular stimuli. Previous studies have suggested that Egr-1 exerts pathological functions in chronic obstructive pulmonary disease (COPD) by regulation of cigarette smoking-induced autophagy, cell death, and inflammation. However, little is known about the role of Egr-1 in regulation of mucus production in airway epithelium.

Neutrophilic Inflammation in the Immune Responses of Chronic Obstructive Pulmonary Disease: Lessons from Animal Models.

Chronic obstructive pulmonary disease (COPD) is a major cause of mortality worldwide, which is characterized by chronic bronchitis, destruction of small airways, and enlargement/disorganization of alveoli. It is generally accepted that the neutrophilic airway inflammation observed in the lungs of COPD patients is intrinsically linked to the tissue destruction and alveolar airspace enlargement, leading to disease progression. Animal models play an important role in studying the underlying mechanisms of COPD as they address questions involving integrated whole body responses.

Autophagy as a double-edged sword in pulmonary epithelial injury: a review and perspective.

Pulmonary epithelial cells form the first line of defense of human airways against foreign irritants and also represent as the primary injury target of these pathogenic assaults. Autophagy is a revolutionary conserved ubiquitous process by which cytoplasmic materials are delivered to lysosomes for degradation when facing environmental and/or developmental changes, and emerging evidence suggests that autophagy plays pivotal but controversial roles in pulmonary epithelial injury. Here we review recent studies focusing on the roles of autophagy in regulating airway epithelial injury induced by various stimuli.

Anatomical Knee Variants in Discoid Lateral Meniscal Tears.

Background: Discoid lateral meniscus was a common meniscal dysplasia and was predisposed to tear. There were some anatomical knee variants in patients with discoid lateral meniscus. The aim of this study was to analyze the relationship between anatomical knee variants and discoid lateral meniscal tears.

Relationship between Inflammatory Response and Estimated Complication Rate after Total Hip Arthroplasty.

Background: After total hip arthroplasty (THA), there is a noteworthy inflammatory response. The inflammatory response is associated with postoperative recovery and complications. However, there had been few reports on the relationship between inflammatory response and postoperative complication rate.

Roles of leptin in bone metabolism and bone diseases.

Adipose tissue has been more accepted as an active contributor to whole body homeostasis, rather than just a fat depot, since leptin, a 16 kDa protein, was discovered as the product of the obese gene in 1994. With more and more studies conducted on this hormone, it has been shown that there is a close relationship between adipose tissue and bone, which have important effects on each other. Bone is the source of many hormones, such as osteocalcin, that can affect energy metabolism and then the anabolism or catabolism of fat tissue.