Submit

Login Login

Register Register

Home / Journals / BIOCELL / Online First / doi:10.32604/biocell.2026.083188
Journal Menu
Special Issues
Table of Content

All issues

Online First

2026

2025

2024

2023

2022

2021

2020

2019

2018

2017

2016

2015

2014

2013

2012

2011

2010

2009

2008

2007

2006

2005

2004

2003

2002

SAIB Annual Meetings

Open Access

REVIEW

Recent Insights into Mitochondrial Dysfunction-Driven Cellular Senescence in Chronic Kidney Disease

Ziyi Guo, Zhenkai Wang, Zixuan Song, Tian Wang, Jingai Fang, Ziyuan Zhang*
Department of Nephrology, The First Hospital of Shanxi Medical University, Shanxi Medical University, Taiyuan, China
* Corresponding Author: Ziyuan Zhang. Email: email
(This article belongs to the Special Issue: Cellular Senescence in Health and Disease)

BIOCELL https://doi.org/10.32604/biocell.2026.083188

Received 30 March 2026; Accepted 25 June 2026; Published online 06 July 2026

Abstract

Chronic kidney disease (CKD) poses a significant global health challenge, with the accumulation of senescent cells contributing to its pathogenesis. This review synthesizes recent advances highlighting mitochondrial dysfunction as a pivotal driver of cellular senescence in CKD progression. We delineate how CKD-specific pathological insults—such as uremic toxins and metabolic stress—compromise mitochondrial integrity, triggering a cascade of interconnected failures: dysregulation of mitochondrial quality control (impaired biogenesis via PGC-1α suppression, disrupted dynamics, and deficient mitophagy) leads to the persistence of damaged organelles. Concurrent bioenergetic decline from compromised oxidative phosphorylation and elevated reactive oxygen species (ROS) production further exacerbates cellular stress. These dysfunctional mitochondria subsequently serve as signaling platforms, activating DNA damage responses and innate immune pathways (e.g., NLRP3 inflammasome, cGAS-STING) that amplify the senescence-associated secretory phenotype (SASP). This process establishes a self-perpetuating cycle of inflammation, paracrine senescence, and fibrosis. Emerging therapeutic strategies focused on restoring mitochondrial homeostasis—including targeted antioxidants, modulators of mitochondrial quality control, and metabolic regulators—show promising results in preclinical models for attenuating renal cellular senescence. Consequently, targeting the mitochondrial-senescence axis offers a novel and compelling therapeutic avenue to mitigate CKD progression.

Keywords

Mitochondrial dysfunction; cellular senescence; chronic kidney disease (CKD); mitochondrial quality control; senescence-associated secretory phenotype (SASP)

  • 226

    View

  • 85

    Download

  • 0

    Like

Related articles
Copyright© 2026 Tech Science Press
© 1997-2026 TSP (Henderson, USA) unless otherwise stated

Share Link