Aging, Cellular Senescence, and Kidney Fibrosis

Abstract

Purpose of Review

Fibrosis is a hallmark of chronic kidney disease, and a primary risk factor for chronic kidney disease is age. Senescent cells accumulate in the kidney during natural aging and after injury. Understanding the effect of senescence on kidney maintenance and how senescence is linked to fibrosis may reveal new therapeutic opportunities.

Recent Findings

The load of senescent cells in the kidney is predictive of biological age and correlates with renal disease and allograft outcome. Senescent cells do not proliferate to repair injury. Instead, they secrete proteins that enhance inflammation and modulate fibrosis. Pharmaceutical blockade of these effects or elimination of senescent cells can counteract age-related disease.

Summary

This review explores the relationships among aging, cellular senescence, inflammation, and kidney fibrosis. Drawing from data from various disciplines, we discuss senescence-associated secretory phenotype, klotho, and senotherapy, analyzing the research and looking for new solutions to age-related kidney fibrosis.

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