Senescence in vascular aging and cardiovascular disease

Vascular biology and geroscience increasingly recognize cellular senescence as an important contributor to vascular aging and cardiovascular disease. Senescent endothelial cells, vascular smooth muscle cells, pericytes, and progenitor cells undergo durable cell-cycle arrest while remaining metabolically active. They can develop a senescence-associated secretory phenotype that releases inflammatory mediators, proteases, and other factors capable of altering the local tissue environment. The accumulation of these cells has been associated with endothelial dysfunction, arterial stiffness, atherosclerotic plaque development, impaired vascular repair, and heart failure. However, senescence is heterogeneous and may vary according to cell type, tissue context, disease stage, and the nature of the initiating stress. Important questions remain regarding how senescent cells interact with immune and vascular systems, how they contribute to plaque progression and instability, and how they can be distinguished from reversibly stressed or dysfunctional cells. Recent preclinical studies suggest that senescence-modulating strategies, including senolytics and senomorphics, may improve vascular outcomes, while advances in multi-omics, imaging, and circulating biomarkers are supporting more precise characterization of senescent cell states and plaque phenotypes. Nevertheless, the translation of these findings to human disease remains limited by incomplete biomarker validation, challenges in identifying clinically relevant senescent-cell populations, and uncertainty regarding therapeutic safety, timing, and target specificity.This Research Topic aims to advance understanding of the cellular and molecular mechanisms linking senescence with vascular aging and atherosclerotic plaque biology. It will examine how senescence is initiated and maintained in vascular cells, how the SASP influences inflammation, thrombosis, vascular remodeling, and heart failure-related vascular pathology, and how senescent cells communicate with immune and parenchymal cells within the vessel wall. The Research Topic will also assess emerging biomarkers and imaging approaches for detecting senescence and vascular aging, and will consider the therapeutic potential of senolytic, senomorphic, metabolic, lifestyle, and regenerative interventions, with emphasis on vascular outcomes. Contributions may address mechanisms, disease associations, therapeutic targets, translational studies, and clinical evidence.To gather further insights into senescence in vascular aging, this Research Topic will focus on cellular, molecular, preclinical, and clinical research, while recognizing that senescence is context-dependent and that biomarker and intervention studies require careful validation. We welcome articles addressing, but not limited to, the following themes:o Molecular mechanisms that induce senescence in endothelial cells, vascular smooth muscle cells, pericytes, progenitor cells, cardiomyocytes, and metabolic tissues.o The role of the senescence-associated secretory phenotype in vascular inflammation, endothelial dysfunction, arterial stiffness, atherosclerosis, thrombosis, and vascular remodeling.o Interactions between cellular senescence, inflammaging, immune responses, oxidative stress, mitochondrial dysfunction, and epigenetic changes.o Biomarkers, imaging methods, and multi-omics approaches for identifying senescent cells and measuring biological vascular age.o Lipid metabolism and lipidomic dysregulation in vascular senescence, including the role of dyslipidemia, lipotoxicity, and altered lipid signaling in driving or accelerating senescent phenotypes in vascular and metabolic tissues.o Experimental models for investigating senescence in vascular and cardiovascular disease.o Senolytic, senomorphic, metabolic, lifestyle, and regenerative strategies for preventing or reversing senescence-associated damage.o Translational studies and clinical trials evaluating senescence-targeted interventions, including their efficacy, safety, timing, and patient selection.o Sex, ancestry, biological age, environmental exposures, and other determinants of heterogeneity in vascular senescence. Topic editors: Junye Chen, Ai Huang, Chaonan Wang Source: https://www.frontiersin.org/research-topics/84855/senescence-in-vascular-aging-and-cardiovascular-disease