ReviewCurrent opinion in nephrology and hypertension2022
Ageing, cellular senescence and chronic kidney disease: experimental evidence.
Review in Current opinion in nephrology and hypertension, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 51 citations in OpenAlex.
- Stage-specific utility of obesity indices across the chronic kidney disease continuum.Renal failure · 2026Article
- Comparative effects of semaglutide tirzepatide and retatrutide on renal fibrosis in UUO and aged mice.iScience · 2026Article
- Senescent Human Liver Endothelial Cells Mediate CD4Immunology · 2026Article
- Calorie Restriction Leads to Degradation of Mutant Uromodulin and Ameliorates Inflammation and Fibrosis in UMOD -Related Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026Article
- Review
- DNA hypermethylation of FGFR2 drives fibrosis in the aging kidney.Scientific reports · 2026Article
- Cellular Senescence Triggered by Food and Environmental Genotoxins.International journal of molecular sciences · 2026Review
- Emerging therapeutic pipelines on kidney fibrosis: challenges in translational research.Journal of translational medicine · 2026Review
- Metabolic reprogramming in diabetes and other endocrine and metabolic disorders: exploring the Warburg effect, ketones, and SGLT2 inhibitors.Reviews in endocrine & metabolic disorders · 2026Review
- Reversing coma by senolytics and stem cells: the future is now.Journal of translational medicine · 2025Review
- Reprogramming cellular senescence and aging clocks for advanced cancer immunotherapy.Molecular cancer · 2025Review
- Dapagliflozin, in addition to ramipril, ameliorates kidney disease progression in mice with Alport syndrome.American journal of physiology. Renal physiology · 2025Article
- Transglutaminase 2-mediated glutamine deamidation enhances p21 stability during senescence.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The boundaries of normal kidney tissue for biomedical research.Current opinion in nephrology and hypertension · 2025Review
- Sendotypes predict worsening renal function in chronic kidney disease patients.Clinical and translational medicine · 2025Article
- PTEN: A Novel Diabetes Nephropathy Protective Gene Related to Cellular Senescence.International journal of molecular sciences · 2025Article
- Acetylation in renal physiology and pathophysiology.Frontiers in pharmacology · 2025Review
- Article
- Chronic kidney disease as a catalyst for cerebral microbleeds: understanding the underlying mechanisms and treatment approaches.Frontiers in medicine · 2025Review
- Adiposity and Mineral Balance in Chronic Kidney Disease.Current osteoporosis reports · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
purpose of reviewChronic kidney disease (CKD) is often viewed as an accelerated and premature ageing of the kidney, as they share common pathological features characterized by cellular senescence. In this review, we summarize the experimental evidence linking cellular senescence to the pathobiology of kidney ageing and CKD, and discuss the strategies for targeting senescent cells in developing therapeutics for ageing-related kidney disorders. RECENT
findingsKidney ageing and CKD are featured with increased cellular senescence, an irreversible state of cell cycle arrest and the cessation of cell division. Senescent cells secrete a diverse array of proinflammatory and profibrotic factors known as senescence-associated secretory phenotype (SASP). Secondary senescence can be induced by primary senescent cells via a mechanism involving direct contact or the SASP. Various senolytic therapies aiming to selectively remove senescent cells in vivo have been developed. Senostatic approaches to suppress senescence or inhibit SASP, as well as nutrient signalling regulators are also validated in animal models of ageing. SUMMARY: These recent studies provide experimental evidence supporting the notion that accumulation of senescent cells and their associated SASP is a main driver leading to structural and functional organ degeneration in CKD and other ageing-related disorder.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.