» Articles » PMID: 36091755

The Interaction Between Cellular Senescence and Chronic Kidney Disease As a Therapeutic Opportunity

Overview
Journal Front Pharmacol
Date 2022 Sep 12
PMID 36091755
Authors
Affiliations
Soon will be listed here.
Abstract

Chronic kidney disease (CKD) is an increasingly serious public health problem in the world, but the effective therapeutic approach is quite limited at present. Cellular senescence is characterized by the irreversible cell cycle arrest, senescence-associated secretory phenotype (SASP) and senescent cell anti-apoptotic pathways (SCAPs). Renal senescence shares many similarities with CKD, including etiology, mechanism, pathological change, phenotype and outcome, however, it is difficult to judge whether renal senescence is a trigger or a consequence of CKD, since there is a complex correlation between them. A variety of cellular signaling mechanisms are involved in their interactive association, which provides new potential targets for the intervention of CKD, and then extends the researches on senotherapy. Our review summarizes the common features of renal senescence and CKD, the interaction between them, the strategies of senotherapy, and the open questions for future research.

Citing Articles

Chronic kidney disease and aging: dissecting the p53/p21 pathway as a therapeutic target.

Goyal K, Afzal M, Altamimi A, Babu M, Ballal S, Kaur I Biogerontology. 2024; 26(1):32.

PMID: 39725742 DOI: 10.1007/s10522-024-10173-z.


Adiposity and Mineral Balance in Chronic Kidney Disease.

Hosain O, Clinkenbeard E Curr Osteoporos Rep. 2024; 22(6):561-575.

PMID: 39394545 DOI: 10.1007/s11914-024-00884-0.


Kidney Aging and Chronic Kidney Disease.

Zhang Y, Yu C, Li X Int J Mol Sci. 2024; 25(12).

PMID: 38928291 PMC: 11204319. DOI: 10.3390/ijms25126585.


Box A of HMGB1 Maintains the DNA Gap and Prevents DDR-induced Kidney Injury in D-galactose Induction Rats.

Khumsri W, Payuhakrit W, Kongkaew A, Chattipakorn N, Chattipakorn S, Yasom S In Vivo. 2024; 38(3):1170-1181.

PMID: 38688613 PMC: 11059889. DOI: 10.21873/invivo.13552.


Risk Factors of Chronic Kidney Disease Progression: Between Old and New Concepts.

Mallamaci F, Tripepi G J Clin Med. 2024; 13(3).

PMID: 38337372 PMC: 10856768. DOI: 10.3390/jcm13030678.


References
1.
Jin H, Zhang Y, Ding Q, Wang S, Rastogi P, Dai D . Epithelial innate immunity mediates tubular cell senescence after kidney injury. JCI Insight. 2019; 4(2). PMC: 6413792. DOI: 10.1172/jci.insight.125490. View

2.
Kidir V, Aynali A, Altuntas A, Inal S, Aridogan B, Sezer M . Telomerase activity in patients with stage 2-5D chronic kidney disease. Nefrologia. 2017; 37(6):592-597. DOI: 10.1016/j.nefro.2017.03.025. View

3.
Yosef R, Pilpel N, Papismadov N, Gal H, Ovadya Y, Vadai E . p21 maintains senescent cell viability under persistent DNA damage response by restraining JNK and caspase signaling. EMBO J. 2017; 36(15):2280-2295. PMC: 5538795. DOI: 10.15252/embj.201695553. View

4.
Liu J, Yang J, Chen X, Cai G, Lin L, He Y . Impact of ER stress-regulated ATF4/p16 signaling on the premature senescence of renal tubular epithelial cells in diabetic nephropathy. Am J Physiol Cell Physiol. 2015; 308(8):C621-30. DOI: 10.1152/ajpcell.00096.2014. View

5.
Li L, Huang L, Ye H, Song S, Bajwa A, Lee S . Dendritic cells tolerized with adenosine A₂AR agonist attenuate acute kidney injury. J Clin Invest. 2012; 122(11):3931-42. PMC: 3484444. DOI: 10.1172/JCI63170. View