Evidence map›Paper›PMID 39139135›Full record

ReviewClinical science (London, England : 1979)2024

To target cellular senescence in diabetic kidney disease: the known and the unknown.

Yuehan Wei, Shan Mou, Qing Yang, Fang Liu, Mark E Cooper, Zhonglin Chai

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Clinical science (London, England : 1979), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  11. Characterization of gut microbiota in patients with diabetic kidney disease.Frontiers in cellular and infection microbiology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Yuehan WeiDepartment of Diabetes, School of Translational Medicine, Monash University, Melbourne, Australia.
Shan MouDepartment of Nephrology, Molecular Cell Laboratory for Kidney Disease, Shanghai Peritoneal Dialysis Research Center, Ren Ji Hospital, Uremia Diagnosis and Treatment Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Qing YangDepartment of Nephrology, Laboratory of Diabetic Kidney Disease, Kidney Research Institute, West China Hospital, Sichuan University, Chengdu, China.
Fang LiuDepartment of Nephrology, Laboratory of Diabetic Kidney Disease, Kidney Research Institute, West China Hospital, Sichuan University, Chengdu, China.ORCID 0000-0003-1121-3004
Mark E CooperDepartment of Diabetes, School of Translational Medicine, Monash University, Melbourne, Australia.
Zhonglin ChaiDepartment of Diabetes, School of Translational Medicine, Monash University, Melbourne, Australia.ORCID 0000-0001-8182-8579

Funding

National Health and Medical Research Council (NHMRC) APP2011355
6 · The paper itself

Abstract

Cellular senescence represents a condition of irreversible cell cycle arrest, characterized by heightened senescence-associated beta-galactosidase (SA-β-Gal) activity, senescence-associated secretory phenotype (SASP), and activation of the DNA damage response (DDR). Diabetic kidney disease (DKD) is a significant contributor to end-stage renal disease (ESRD) globally, with ongoing unmet needs in terms of current treatments. The role of senescence in the pathogenesis of DKD has attracted substantial attention with evidence of premature senescence in this condition. The process of cellular senescence in DKD appears to be associated with mitochondrial redox pathways, autophagy, and endoplasmic reticulum (ER) stress. Increasing accumulation of senescent cells in the diabetic kidney not only leads to an impaired capacity for repair of renal injury, but also the secretion of pro-inflammatory and profibrotic cytokines and growth factors causing inflammation and fibrosis. Current treatments for diabetes exhibit varying degrees of renoprotection, potentially via mitigation of senescence in the diabetic kidney. Targeting senescent cell clearance through pharmaceutical interventions could emerge as a promising strategy for preventing and treating DKD. In this paper, we review the current understanding of senescence in DKD and summarize the possible therapeutic interventions relevant to senescence in this field.

Indexed as

Cellular SenescenceDiabetic NephropathiesAnimalsAutophagyEndoplasmic Reticulum StressHumansKidneySenescence-Associated Secretory PhenotypeCellular Senescencediabetic nephropathyinlfammationrenal fibrosis

Identifiers

PMID39139135
PMCPMC11327223

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Registered trials

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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.