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Replicative Cell Senescence

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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...

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Related Experiment Video

Updated: Jul 4, 2026

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs

Published on: June 28, 2019

Renal senescence in 2008: progress and challenges.

Xin J Zhou¹, Ramesh Saxena, Zhihong Liu

¹Department of Pathology, UT Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9073, USA. joseph.zhou@utsouthwestern.edu

International Urology and Nephrology

|June 28, 2008

Summary

Kidney function declines with aging due to anatomic and functional changes, increasing risks for the elderly. Understanding key aging mechanisms like oxidative stress and the renin-angiotensin system is crucial for preserving renal health.

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Induction and Validation of Cellular Senescence in Primary Human Cells

Induction and Validation of Cellular Senescence in Primary Human Cells

Published on: June 20, 2018

Area of Science:

Nephrology
Gerontology
Molecular Biology

Background:

Kidney structure and function undergo significant changes with aging (senescence).
These age-related kidney changes predispose older adults to drug toxicity and fluid/electrolyte imbalances.
Key molecular mechanisms implicated in kidney aging include oxidative stress, telomere shortening, Klotho gene expression, and the renin-angiotensin system.

Purpose of the Study:

To explore the complex molecular pathways involved in kidney aging.
To understand the clinical implications of aging on renal function.
To identify mechanisms that could be targeted for intervention.

Main Methods:

Review of current literature on kidney aging mechanisms.
Analysis of molecular pathways such as oxidative stress, telomere length, Klotho, and renin-angiotensin system.
Focus on the interplay between multiple molecular pathways.

Main Results:

Aging leads to reduced glomerular filtration rate, impaired urinary concentration, acidification, and potassium handling.
Oxidative stress, telomere attrition, altered Klotho expression, and renin-angiotensin system dysregulation are central to kidney aging.
Studying these pathways in parallel offers insights into kidney aging's progression.

Conclusions:

A comprehensive understanding of kidney aging mechanisms is essential for improving health outcomes in the elderly.
Targeting these molecular pathways may help preserve renal function and reduce age-related morbidity and mortality.
Further research into these intertwined pathways can inform strategies to mitigate kidney aging and associated healthcare costs.