ArticleKidney international2013
Thymosin β4 and its degradation product, Ac-SDKP, are novel reparative factors in renal fibrosis.
Article in Kidney international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 88 citations in OpenAlex.
- 0.1% RGN-259 (Thymosin ß4) Ophthalmic Solution Promotes Healing and Improves Comfort in Neurotrophic Keratopathy Patients in a Randomized, Placebo-Controlled, Double-Masked Phase III Clinical Trial.International journal of molecular sciences · 2022Trial
- Prenatal body fluid analysis in the evaluation of CAKUT.Pediatric nephrology (Berlin, Germany) · 2026Review
- Article
- Exploring disulfiram mechanisms in renal fibrosis: insights from biological data and computational approaches.Frontiers in pharmacology · 2025Article
- The secreted micropeptide C4orf48 enhances renal fibrosis via an RNA-binding mechanism.The Journal of clinical investigation · 2024Article
- Association of serum thymosin β4 with malnutrition-inflammation-atherosclerosis syndrome in peritoneal dialysis patients: a cross-sectional study.Renal failure · 2023Article
- Article
- The Pathophysiological Role of Thymosin β4 in the Kidney Glomerulus.International journal of molecular sciences · 2023Review
- Cell surface GRP78 regulates TGFβ1-mediated profibrotic responsesFrontiers in pharmacology · 2023Article
- The Role of Tβ4-POP-Ac-SDKP Axis in Organ Fibrosis.International journal of molecular sciences · 2022Review
- Systemic gene therapy with thymosin β4 alleviates glomerular injury in mice.Scientific reports · 2022Article
- Urine peptidome analysis in cardiorenal syndrome reflects molecular processes.Scientific reports · 2021Article
- Early Renoprotective Effect of Ruxolitinib in a Rat Model of Diabetic Nephropathy.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Progress on the Function and Application of Thymosin β4.Frontiers in endocrinology · 2021Review
- CD-1Journal of diabetes investigation · 2020Article
- N-acetyl-seryl-aspartyl-lysyl-proline is a valuable endogenous antifibrotic peptide for kidney fibrosis in diabetes: An update and translational aspects.Journal of diabetes investigation · 2020Review
- Thymosin β4-Enhancing Therapeutic Efficacy of Human Adipose-Derived Stem Cells in Mouse Ischemic Hindlimb Model.International journal of molecular sciences · 2020Article
- Ang II (Angiotensin II) Conversion to Angiotensin-(1-7) in the Circulation Is POP (Prolyloligopeptidase)-Dependent and ACE2 (Angiotensin-Converting Enzyme 2)-Independent.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Diabetic Nephropathy: Novel Molecular Mechanisms and Therapeutic Targets.Frontiers in pharmacology · 2020Review
- Tβ4-Ac-SDKP pathway: Any relevance for the cardiovascular system?Canadian journal of physiology and pharmacology · 2019Review
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 5 countries.
Funding
Abstract
Previously, we found thymosin β4 (Tβ4) is upregulated in glomerulosclerosis and required for angiotensin II-induced expression of plasminogen activator inhibitor-1 (PAI-1) in glomerular endothelial cells. Tβ4 has beneficial effects in dermal and corneal wound healing and heart disease, yet its effects in kidney disease are unknown. Here we studied renal fibrosis in wild-type and PAI-1 knockout mice following unilateral ureteral obstruction to explore the impact of Tβ4 and its prolyl oligopeptidase tetrapeptide degradation product, N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), in renal fibrosis. Additionally, we explored interactions of Tβ4 with PAI-1. Treatment with Ac-SDKP significantly decreased fibrosis in both wild-type and PAI-1 knockout mice, as observed by decreased collagen and fibronectin deposition, fewer myofibroblasts and macrophages, and suppressed profibrotic factors. In contrast, Tβ4 plus a prolyl oligopeptidase inhibitor significantly increased fibrosis in wild-type mice. Tβ4 alone also promoted repair and reduced late fibrosis in wild-type mice. Importantly, both profibrotic effects of Tβ4 plus the prolyl oligopeptidase inhibitor, and late reparative effects of Tβ4 alone, were absent in PAI-1 knockout mice. Thus, Tβ4 combined with prolyl oligopeptidase inhibition is consistently profibrotic, but by itself has antifibrotic effects in late-stage fibrosis, while Ac-SDKP has consistent antifibrotic effects in both early and late stages of kidney injury. These effects of Tβ4 are dependent on PAI-1.
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Registered trials
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