ArticleClinical science (London, England : 1979)2024
Intervention treatment reducing cellular senescence inhibits tubulointerstitial fibrosis in diabetic mice following acute kidney injury.
Article 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 18 papers.
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Who cites it
18 citing papers in PubMed, 15 citations in OpenAlex.
- Acute renal injury in ANCA-associated glomerulonephritis: etiology related to acute tubulointerstitial injury versus glomerular injury.Renal failure · 2026Article
- The oocyte-enriched metabolite serotonin alleviates cellular senescence and aging phenotypes in the mouse.The EMBO journal · 2026Article
- Knocking Down CDKN2A Enhances the Therapeutic Effects of Metformin and Resveratrol on Diabetic Retinopathy.Applied biochemistry and biotechnology · 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
- Mechanistic insights into SOCS5-related DNA damage and cellular senescence in diabetic retinopathy.Cell death discovery · 2026Article
- Targeting cellular senescence in diabetic kidney disease: potential of regenerative, cell-based therapies and other senotherapeutic approaches.Kidney international · 2026Review
- Integrative Approaches to Treating Cellular Senescence in Kidney Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Cellular senescence of renal tubular epithelial cells in diabetic kidney disease: emerging mechanisms and targeted interventions.Frontiers in cell and developmental biology · 2026Review
- Integrative Transcriptomics Across Etiologies Reveals Common and Disease-Specific Fibrogenic Signatures in Liver Fibrosis.Canadian journal of gastroenterology & hepatology · 2026Article
- Deficiency of mineralocorticoid receptor signalling in myeloid cells protects cardiac and kidney function in hypertensive diabetic mice.Clinical science (London, England : 1979) · 2025Article
- Multi-target regulation of cellular senescence by traditional Chinese medicine: a novel strategy to preventing diabetic kidney disease.Renal failure · 2025Review
- Unraveling the meta-hallmarks between senescent and tumor cells: A new perspective for senolytic drug discovery.Acta pharmaceutica Sinica. B · 2025Review
- Cellular senescence in renal ischemia-reperfusion injury.Chinese medical journal · 2025Review
- Therapy-induced senescence is a transient drug resistance mechanism in breast cancer.Molecular cancer · 2025Article
- Targeting senescence to prevent diabetic kidney disease: Exploring molecular mechanisms and potential therapeutic targets for disease management.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- A new Jun amino-terminal kinase inhibitor, KRev-202, inhibits rat ischemic acute injury and the progression to renal fibrosis.Frontiers in pharmacology · 2025Article
- Role of inflammation-related genes as prognostic biomarkers and mechanistic implications in idiopathic pulmonary fibrosis.Frontiers in genetics · 2025Article
- To target cellular senescence in diabetic kidney disease: the known and the unknown.Clinical science (London, England : 1979) · 2024Review
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4 authors at 1 institution in 1 country.
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Abstract
Senescence of kidney tubules leads to tubulointerstitial fibrosis (TIF). Proximal tubular epithelial cells undergo stress-induced senescence during diabetes and episodes of acute kidney injury (AKI), and combining these injuries promotes the progression of diabetic kidney disease (DKD). Since TIF is crucial to progression of DKD, we examined the therapeutic potential of targeting senescence with a senolytic drug (HSP90 inhibitor) and/or a senostatic drug (ASK1 inhibitor) in a model of TIF in which AKI is superimposed on diabetes. After 8 weeks of streptozotocin-induced diabetes, mice underwent bilateral clamping of renal pedicles to induce mild AKI, followed by 28 days of reperfusion. Groups of mice (n=10-12) received either vehicle, HSP90 inhibitor (alvespimycin), ASK1 inhibitor (GS-444217), or both treatments. Vehicle-treated mice displayed tubular injury at day 3 and extensive tubular cell senescence at day 10, which remained unresolved at day 28. Markers of senescence (Cdkn1a and Cdkn2a), inflammation (Cd68, Tnf, and Ccl2), and TIF (Col1a1, Col4a3, α-Sma/Acta2, and Tgfb1) were elevated at day 28, coinciding with renal function impairment. Treatment with alvespimycin alone reduced kidney senescence and levels of Col1a1, Acta2, Tgfb1, and Cd68; however, further treatment with GS-444217 also reduced Col4a3, Tnf, Ccl2, and renal function impairment. Senolytic therapy can inhibit TIF during DKD, but its effectiveness can be improved by follow-up treatment with a senostatic inhibitor, which has important implications for treating progressive DKD.
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