Diabetic kidney disease (DKD) remains a leading cause of end-stage renal disease worldwide, characterized by increasing prevalence and limited therapeutic options. This review comprehensively synthesizes recent advances in the molecular mechanisms underlying DKD progression, focusing on key cellular events including podocyte injury, tubular damage, endothelial dysfunction, pericyte loss, and immune-inflammatory responses that drive glomerular and tubulointerstitial fibrosis. We further elaborate on critical pathways such as lipotoxicity, mitochondrial dysfunction and oxidative stress, aberrant autophagy, inflammasome activation, and profibrotic signaling.

Hemophagocytic lymphohistiocytosis (HLH) is a rare and life-threatening disease characterized by immune overstimulation and hyperinflammatory response.[1] Although the prognosis is poor, with a high mortality rate of up to 58% in critically ill patients,[2] the treatment for HLH is potentially curative. Active HLH treatment involves immunosuppressive induction therapy, followed by hematopoietic stem-cell transplant (HSCT).

Depression affects at least 300 million people globally to varying degrees and is projected to be the number one disorder in terms of disability and disease burden by 2030.[1] Among university students, depressive symptoms are mostly manifested as a sub-healthy state characterized by low mood, despair, nervousness, and even suicidal intentions. At present, the detection rate of depressive symptoms among college students is much higher than that of other groups, with a year-by-year upward trend.

Previous studies have confirmed that chondrocytes are derived from mesenchymal stem cells (MSCs) and mature into hypertrophic chondrocytes during endochondral ossification. This maturation is followed by apoptosis, which induces vascular invasion, cartilage matrix degradation, and osteoblast differentiation. In addition to this classical transdifferentiation pathway, recent studies have shown that chondrocytes can also be derived from periosteal stem cells (PSCs).