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

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. Significance statement: The present work is aimed at understanding the interactions between cellular senescence and inflamm‐aging that together predispose the elderly to recurring infections and inflammatory disorders. The rationale for viewing these two processes together with their interdependent pathophysiology has been presented. This paper intends to apprise the scientific community of this developing interconnection and underlying disease pathology that may ultimately help identify novel molecular markers and therapeutic targets of inflammatory disorders during aging. [ABSTRACT FROM AUTHOR]