Abstract

Cellular senescence is one type of permeant arrest of cell growth and one of increasingly recognized contributor to aging and age-associated disease. High phosphate and low Klotho individually and synergistically lead to age-related degeneration in multiple organs. Substantial evidence supports the causality of high phosphate in cellular senescence, and potential contribution to human aging, cancer, cardiovascular, kidney, neurodegenerative, and musculoskeletal diseases. Phosphate can induce cellular senescence both by direct phosphotoxicity, and indirectly through downregulation of Klotho and upregulation of plasminogen activator inhibitor-1. Restriction of dietary phosphate intake and blockage of intestinal absorption of phosphate help suppress cellular senescence. Supplementation of Klotho protein, cellular senescence inhibitor, and removal of senescent cells with senolytic agents are potential novel strategies to attenuate phosphate-induced cellular senescence, retard aging, and ameliorate age-associated, and phosphate-induced disorders.

Original languageEnglish (US)
Title of host publicationAdvances in Experimental Medicine and Biology
PublisherSpringer
Pages55-72
Number of pages18
DOIs
StatePublished - 2022

Publication series

NameAdvances in Experimental Medicine and Biology
Volume1362
ISSN (Print)0065-2598
ISSN (Electronic)2214-8019

Keywords

  • Age-associated disease
  • Aging
  • Cellular senescence
  • Fibrosis
  • Klotho
  • Phosphate
  • Phosphorus
  • Phosphotoxicity
  • Plasminogen activator inhibitor-1
  • p16
  • p21

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Fingerprint

Dive into the research topics of 'Phosphate and Cellular Senescence'. Together they form a unique fingerprint.

Cite this