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Updated: Feb 14, 2026
Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
Cellular senescence as a therapeutic target to improve renal transplantation outcome
Hester van Willigenburg1, Peter L J de Keizer2, Ron W F de Bruin3
1Department of Molecular Genetics, Erasmus University Medical Center, Rotterdam, The Netherlands; Department of Surgery, Erasmus University Medical Center, Rotterdam, The Netherlands.
Abstract:
Kidney transplants from aged donors are more vulnerable to ischemic injury, suffer more from delayed graft function and have a lower graft survival compared to kidneys from younger donors. On a cellular level, aging results in an increase in cells that are in a permanent cell cycle arrest, termed senescence, which secrete a range of pro-inflammatory cytokines and growth factors. Consequently, these senescent cells negatively influence the local milieu by causing inflammaging, and by reducing the regenerative capacity of the kidney. Moreover, the oxidative damage that is inflicted by ischemia-reperfusion injury during transplantation can induce senescence and accelerate aging. In this review, we describe recent developments in the understanding of the biology of aging that have led to the development of a new class of therapeutic agents aimed at eliminating senescent cells. These compounds have already shown to be able to restore tissue homeostasis in old mice, improve kidney function and general health- and lifespan. Use of these anti-senescence compounds holds great promise to improve the quality of marginal donor kidneys as well as to remove senescent cells induced by ischemia-reperfusion injury. Altogether, senescent cell removal may increase the donor pool, relieving the growing organ shortage and improve long-term transplantation outcome.
Insights
Eliminating senescent cells, which accumulate with age and cause kidney damage, can improve transplant outcomes. This approach shows promise for enhancing kidney function and extending lifespan in aged individuals.
Area of Science:
- Gerontology
- Transplantation immunology
- Cellular biology
Background:
- Kidney transplants from aged donors exhibit increased vulnerability to ischemic injury, delayed graft function, and reduced graft survival.
- Cellular senescence, characterized by permanent cell cycle arrest, increases with age and contributes to inflammaging and diminished regenerative capacity.
- Ischemia-reperfusion injury during transplantation can induce senescence, exacerbating kidney aging and dysfunction.
Purpose of the Study:
- To review recent advancements in understanding aging biology and the development of senolytic therapies.
- To explore the potential of senescent cell elimination to improve kidney transplantation outcomes.
- To discuss the implications of senolytics for marginal donor kidney quality and ischemia-reperfusion injury.
Main Methods:
- Literature review of aging biology and senolytic therapeutic development.
- Analysis of studies investigating the effects of senescent cell removal in aged animal models.
- Examination of the impact of senolytics on kidney function and transplantation.
Main Results:
- Senescent cells contribute to kidney aging and dysfunction through inflammaging and reduced regeneration.
- Senolytic compounds have demonstrated efficacy in restoring tissue homeostasis and improving kidney function in aged mice.
- These therapies show potential for enhancing healthspan and lifespan.
Conclusions:
- Senescent cell removal offers a promising strategy to improve the quality of marginal donor kidneys.
- Targeting senescent cells can mitigate damage from ischemia-reperfusion injury in transplantation.
- Eliminating senescent cells may expand the donor pool and enhance long-term transplant success.
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