ArticleBMJ open diabetes research & care2019
Senescence marker activin A is increased in human diabetic kidney disease: association with kidney function and potential implications for therapy.
Article in BMJ open diabetes research & care, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Association and causality between diabetes and activin A: a two-sample Mendelian randomization study.Frontiers in endocrinology · 2024Pooled it
- A compendium of circulating biomarkers of senescence in humans: Insights on mechanistic impact across health domains and modulation by therapeutic interventions.Ageing research reviews · 2026Review
- Serum activin A and bone metabolism in patients undergoing hemodialysis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026Article
- Circulating cell type senescence signatures track distinct dimensions of health status and trajectories in human longitudinal cohorts.Cell reports · 2026Article
- Molecular mechanisms and therapeutic strategies of glomerular cell senescence in diabetic kidney disease: from heterogeneity to precision intervention.Cellular and molecular life sciences : CMLS · 2026Review
- Targeting cellular senescence in diabetic kidney disease: potential of regenerative, cell-based therapies and other senotherapeutic approaches.Kidney international · 2026Review
- Circulating Cell Type Senescence Signatures Reveal High-Resolution Health Status and Trajectories in Human Longitudinal Studies.medRxiv : the preprint server for health sciences · 2026Article
- miR-299a-5p is a mediator of fibrosis in diabetic kidney disease by regulating follistatin and cripto-1.Communications biology · 2025Article
- Inhibition of Activin A Signaling by Follistatin Alleviates Diabetic Kidney Disease Burden.Kidney360 · 2025Article
- Cellular senescence in adult pulmonary hypertension: current state and future challenges.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Type 2 Diabetes Mellitus: A Metabolic Model of Accelerated Aging - Multi-Organ Mechanisms and Intervention Approaches.Aging and disease · 2025Review
- Article
- Analysis of TGFβ1-Induced activin A gene expression in kidney mesangial cells.Frontiers in molecular biosciences · 2025Article
- Targeting Cell Senescence and Senolytics: Novel Interventions for Age-Related Endocrine Dysfunction.Endocrine reviews · 2024Review
- Activin A plays an essential role in migration and proliferation of hepatic stellate cells via Smad3 and calcium signaling.Scientific reports · 2024Article
- To target cellular senescence in diabetic kidney disease: the known and the unknown.Clinical science (London, England : 1979) · 2024Review
- In chronic kidney disease altered cardiac metabolism precedes cardiac hypertrophy.American journal of physiology. Renal physiology · 2024Article
- White adipocyte dysfunction and obesity-associated pathologies in humans.Nature reviews. Molecular cell biology · 2024Review
- Cellular senescence of renal tubular epithelial cells in acute kidney injury.Cell death discovery · 2024Review
- Diminished vasculogenesis under inflammatory conditions is mediated by Activin A.Angiogenesis · 2023Article
Corrections and comments
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Authors and funding
20 authors at 4 institutions in 3 countries.
Funding
Abstract
Objective: Activin A, an inflammatory mediator implicated in cellular senescence-induced adipose tissue dysfunction and profibrotic kidney injury, may become a new target for the treatment of diabetic kidney disease (DKD) and chronic kidney diseases. We tested the hypothesis that human DKD-related injury leads to upregulation of activin A in blood and urine and in a human kidney cell model. We further hypothesized that circulating activin A parallels kidney injury markers in DKD. Research design and methods: In two adult diabetes cohorts and controls (Minnesota, USA; Galway, Ireland), the relationships between plasma (or urine) activin A, estimated glomerular filtration rate (eGFR) and DKD injury biomarkers were tested with logistic regression and correlation coefficients. Activin A, inflammatory, epithelial-mesenchymal-transition (EMT) and senescence markers were assayed in human kidney (HK-2) cells incubated in high glucose plus transforming growth factor-β1 or albumin. Results: Plasma activin A levels were elevated in diabetes (n=206) compared with controls (n=76; 418.1 vs 259.3 pg/mL; p<0.001) and correlated inversely with eGFR (r Conclusions: Circulating activin A is increased in human DKD and correlates with reduced kidney function and kidney injury markers. DKD-injured human renal tubule cells develop a profibrotic and inflammatory phenotype with activin A upregulation. These findings underscore the role of inflammation and provide a basis for further exploration of activin A as a diagnostic marker and therapeutic target in DKD.
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