Sustained exposure to high glucose induces differential expression of cellular senescence markers in murine macrophages but impairs immunosurveillance response to senescent cells secretome

Diwan, Bhawna; Yadav, Rahul; Goyal, Rohit; Sharma, Rohit

doi:10.1007/s10522-024-10092-z

Cited by 4 publications

(1 citation statement)

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“…109 In another recent study, we observed that hyperglycemia exposed murine macrophages develop a pro-inflammatory and impaired immunosurveillance response when exposed to SASP of senescent preadipocytes. 110 T cell senescence was accompanied by SASP that exacerbated neuroinflammation and tumorigenesis in experimental mice. 111 Exposure to conditioned media derived from SASP-expressing senescent fibroblasts induced pyroptosis in mammary epithelial cells.…”

Section: Cellular Senescence Augments Inflamm-agingmentioning

confidence: 99%

Exploring the emerging bidirectional association between inflamm‐aging and cellular senescence in organismal aging and disease

Sharma

2024

Cell Biochemistry & Function

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There is strong evidence that most individuals in the elderly population are characterized by inflamm‐aging which refers to a subtle increase in the systemic pro‐inflammatory environment and impaired innate immune activation. Although a variety of distinct factors are associated with the progression of inflamm‐aging, emerging research is demonstrating a dynamic relationship between the processes of cellular senescence and inflamm‐aging. Cellular senescence is a recognized factor governing organismal aging, and through a characteristic secretome, accumulating senescent cells can induce and augment a pro‐inflammatory tissue environment that provides a rationale for immune system‐independent activation of inflamm‐aging and associated diseases. There is also accumulating evidence that inflamm‐aging or its components can directly accelerate the development of senescent cells and ultimately senescent cell burden in tissues in a likely vicious inflammatory loop. The present review is intended to describe the emerging senescence‐based molecular etiology of inflamm‐aging as well as the dynamic reciprocal interactions between inflamm‐aging and cellular senescence. Therapeutic interventions concurrently targeting cellular senescence and inflamm‐aging are discussed and limitations as well as research opportunities have been deliberated. An effort has been made to provide a rationale for integrating inflamm‐aging with cellular senescence both as an underlying cause and therapeutic target for further studies.

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Section: Cellular Senescence Augments Inflamm-agingmentioning

confidence: 99%