Cellular senescence is a state of permanent cell cycle arrest and plays an important role in many vascular lesions. This study found that the cells of diabetic patients have more characteristics of senescence, which may cause microvascular complications. Cell senescence, as one of the common fates of cells, links microangiopathy and diabetes. Cell senescence in a high-glucose environment can partially elucidate the mechanism of diabetic microangiopathy, and various types of cellular senescence induced by it can promote the progression of diabetic microangiopathy. Still, the molecular mechanism of microangiopathy-related cellular senescence has not yet been clearly studied. Building on recent research evidence, we herein summarize the fundamental mechanisms underlying the development of cellular senescence in various microangiopathies associated with diabetes. We gradually explain how cellular senescence serves as a key driver of diabetic microangiopathy. At the same time, the treatment of basic senescence mechanisms such as cellular senescence may have a great impact on the pathogenesis of the disease, may be more effective in preventing the development of diabetic microangiopathy, and may provide new ideas for the clinical treatment and prognosis of diabetic microangiopathy.

Age-related macular degeneration (AMD), the leading cause of irreversible blindness worldwide, represents a complex neurodegenerative disorder whose pathogenesis remains elusive. At the core of AMD pathophysiology lies the retinal pigment epithelium (RPE), whose epithelial–mesenchymal transition (EMT) has emerged as a critical pathological mechanism driving disease progression. This transformative process, characterized by RPE cell dedifferentiation and subsequent extracellular matrix remodeling, is orchestrated through a sophisticated network of molecular interactions and cellular signaling cascades. Our review provides a comprehensive analysis of the molecular landscape underlying RPE EMT in AMD, with particular emphasis on seven interconnected pathological axes: (i) oxidative stress and mitochondrial dysfunction, (ii) hypoxia-inducible factor signaling, (iii) autophagic flux dysregulation, (iv) chronic inflammatory responses, (v) complement system overactivation, (vi) epigenetic regulation through microRNA networks, and (vii) key developmental signaling pathway reactivation. Furthermore, we evaluate emerging therapeutic strategies targeting EMT modulation, providing a comprehensive perspective on potential interventions to halt AMD progression. By integrating current mechanistic insights with therapeutic prospects, this review aims to bridge the gap between fundamental research and clinical translation in AMD management.

Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by the destruction of insulin-producing β-cells. Emerging evidence highlights the pivotal role of CD4+ T cell subsets in driving T1D pathogenesis, where their activation, proliferation, and differentiation are tightly regulated by glucose metabolic pathways. Recent studies demonstrate that key enzymes and intermediates of glycolysis, OXPHOS, and other metabolic pathways critically modulate CD4+ T cell functions. In this review, we discuss how glucose metabolic pathways affect CD4+ T cell differentiation and functions. We also summarize the latest progress regarding glucose metabolism intervention to control the T cell immune response in T1D, with the expectation of providing new insights into T1D progression and treatment.

Micro- and nanoplastics (MNPs) are emerging environmental pollutants, but evidence concerning their effects on endometrial injury and adverse pregnancy outcomes remains limited. Therefore, we employed the Targeted Risk Assessment of Environmental Chemicals (TRAEC) strategy to integrate evidence concerning endometrial injury and adverse pregnancy outcomes associated with exposure to MNPs. Following targeted screening, 21 unique studies yielded 24 literature-derived evidence entries. Together with one additional in vitro evidence item from the present study, 25 evidence items were included in the final CES calculation. The available evidence was quantitatively integrated across four predefined TRAEC dimensions: Reliability Scores, Weight of Concentrations, Risk Intensity, and Correlation Scores. Under the tested in vitro conditions, exposure to PS-NPs increased intracellular ROS accumulation, reduced mitochondrial membrane potential, promoted apoptosis, and decreased the expression of key endometrial receptivity proteins, namely HOXA10, FOXO1, and ITGB3, in primary human endometrial stromal cells. Based on this combined evidence pool, the final Comprehensive Evidence Score was 7.67, corresponding to a preliminary moderate-risk classification within the predefined TRAEC framework. In summary, the TRAEC strategy provides a structured approach for integrating multi-level evidence and deriving a framework-specific health-risk classification for exposure to MNPs.