ReviewOncotarget2017
Cellular senescence, senescence-associated secretory phenotype, and chronic kidney disease.
Review in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
81 citing papers in PubMed, 113 citations in OpenAlex.
- Renal Tubular Epithelial Cells Senescence Induced by 1-Aminopyrene Activates Fibroblast via BRD4 Driven Senescence-Associated Secretory Phenotype Signaling.Journal of biochemical and molecular toxicology · 2026Article
- Cellular senescence and inflammageing: from mechanisms to senotherapeutic interventions.Biogerontology · 2026Review
- Deciphering the impact ofGenes & diseases · 2026Article
- Exploratory study of dialysis membrane impact on epigenetic methylation patterns in hemodialysis patients using genomic and synchrotron investigations.Scientific reports · 2026Article
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- Chronic Kidney Disease and Cellular Senescence.International journal of molecular sciences · 2026Review
- Alterations in mitochondria and cellular senescence in aged sEH null female kidneys.GeroScience · 2026Article
- The biology of PKM2 in the metabolism and senescence in diabetic kidney disease.Journal of diabetes investigation · 2026Review
- Review
- Progress in the study of the role of C5a-induced tubular cell senescence in the progression of diabetic kidney disease.Annals of medicine · 2025Review
- Association between a history of hypothyroidism and incident chronic kidney disease and potential mediators: A cohort study with Mendelian randomization analysis.The Journal of international medical research · 2025Article
- Understanding and targeting senescence in kidney disease.Clinical kidney journal · 2025Review
- Decoding diabetic kidney disease: a comprehensive review of interconnected pathways, molecular mediators, and therapeutic insights.Diabetology & metabolic syndrome · 2025Review
- Nfkb1 Removal from Proximal Tubule Cells Improves Renal Tubular Outcomes Following Ischemia Reperfusion Injury.Kidney360 · 2025Article
- Ethnicity-specific patterns of epigenetic age acceleration in rheumatoid arthritis.GeroScience · 2025Article
- On the Path to a Sustainable Diet: Native Brazilian Fruits of the Caryocar spp. (Pequi and Piquiá) and Potential Health Benefits in Chronic Kidney Disease.Plant foods for human nutrition (Dordrecht, Netherlands) · 2025Review
- Purinoreceptor P2X7 in Extracellular ATP-Mediated Inflammation through the Spectrum of Kidney Diseases and Kidney Transplantation.Journal of the American Society of Nephrology : JASN · 2025Review
- The relationship between telomere length and aging-related diseases.Clinical and experimental medicine · 2025Review
- Pathophysiology of vascular ageing and the effect of novel cardio-renal protective medications in preventing progression of chronic kidney disease in people living with diabetes.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- Article
21 more citing papers are in PubMed but not listed here.
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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic kidney disease (CKD) is increasingly being accepted as a type of renal ageing. The kidney undergoes age-related alterations in both structure and function. To date, a comprehensive analysis of cellular senescence and senescence-associated secretory phenotype (SASP) in CKD is lacking. Hence, this review mainly discusses the relationship between the two phenomena to show the striking similarities between SASP and CKD-associated secretory phenotype (CASP). It has been reported that replicative senescence, stress-induced premature ageing, and epigenetic abnormalities participate in the occurrence and development of CKD. Genomic damage and external environmental stimuli cause increased levels of oxidative stress and a chronic inflammatory state as a result of irreversible cell cycle arrest and low doses of SASP. Similar to SASP, CASP factors activate tissue repair by multiple mechanisms. Once tissue repair fails, the accumulated SASP or CASP species aggravate DNA damage response (DDR) and cause the senescent cells to secrete more SASP factors, accelerating the process of cellular ageing and eventually leading to various ageing-related changes. It is concluded that cellular senescence and SASP participate in the pathological process of CKD, and correspondingly CKD accelerated the progression of cell senescence and the secretion of SASP. These results will facilitate the integration of these mechanisms into the care and management of CKD and other age-related diseases.
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What OpenQuestion holds
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.