ArticlePloS one2016
Novel Plasminogen Activator Inhibitor-1 Inhibitors Prevent Diabetic Kidney Injury in a Mouse Model.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Optimizing diabetic kidney disease animal models: Insights from a meta-analytic approach.Animal models and experimental medicine · 2023Pooled it
- Review
- Plasminogen activator inhibitor-1 as an oncologic target: biology, therapeutic inhibitors, and clinical translation.Frontiers in oncology · 2026Review
- Pathogenic and Regulatory Roles of Fibrinolytic Factors in Autoimmune Diseases.Current issues in molecular biology · 2025Review
- Palmitic Acid Accelerates Endothelial Cell Injury and Cardiovascular Dysfunction via Palmitoylation of PKM2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Hypermethylation and suppression of microRNA219a-2 activates the ALDH1L2/GSH/PAI-1 pathway for fibronectin degradation in renal fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- CUL4B protects kidneys from acute injury by restraining p53/PAI-1 signaling.Cell death & disease · 2024Article
- Chemical Adjustment of Fibrinolysis.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Role of plasminogen activated inhibitor-1 in the pathogenesis of anticoagulant related nephropathy.Frontiers in nephrology · 2024Article
- Article
- Serpin E1 mediates the induction of renal tubular degeneration and premature senescence upon diabetic insult.Scientific reports · 2023Article
- Prevention strategies of postoperative adhesion in soft tissues by applying biomaterials: Based on the mechanisms of occurrence and development of adhesions.Bioactive materials · 2023Review
- Molecular profiling of the stroke-induced alterations in the cerebral microvasculature reveals promising therapeutic candidates.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Potentials of ketogenic diet against chronic kidney diseases: pharmacological insights and therapeutic prospects.Molecular biology reports · 2022Review
- Renoprotective Effects of Mangiferin: Pharmacological Advances and Future Perspectives.International journal of environmental research and public health · 2022Review
- Kidney protective potential of lactoferrin: pharmacological insights and therapeutic advances.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Review
- The Astragaloside IV Derivative LS-102 Ameliorates Obesity-Related Nephropathy.Drug design, development and therapy · 2022Article
- PAI-1 in Diabetes: Pathophysiology and Role as a Therapeutic Target.International journal of molecular sciences · 2021Review
- Postoperative peritoneal adhesion: an update on physiopathology and novel traditional herbal and modern medical therapeutics.Naunyn-Schmiedeberg's archives of pharmacology · 2021Review
- Protective Effects of Eicosapentaenoic Acid on the Glomerular Endothelium via Inhibition of EndMT in Diabetes.Journal of diabetes research · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy is the leading cause of end-stage renal disease worldwide, but no effective therapeutic strategy is available. Because plasminogen activator inhibitor-1 (PAI-1) is increasingly recognized as a key factor in extracellular matrix (ECM) accumulation in diabetic nephropathy, this study examined the renoprotective effects of TM5275 and TM5441, two novel orally active PAI-1 inhibitors that do not trigger bleeding episodes, in streptozotocin (STZ)-induced diabetic mice. TM5275 (50 mg/kg) and TM5441 (10 mg/kg) were administered orally for 16 weeks to STZ-induced diabetic and age-matched control mice. Relative to the control mice, the diabetic mice showed significantly increased (p < 0.05) plasma glucose and creatinine levels, urinary albumin excretion, kidney-to-bodyweight ratios, glomerular volume, and fractional mesangial area. Markers of fibrosis and inflammation along with PAI-1 were also upregulated in the kidney of diabetic mice, and treatment with TM5275 and TM5441 effectively inhibited albuminuria, mesangial expansion, ECM accumulation, and macrophage infiltration in diabetic kidneys. Furthermore, in mouse proximal tubular epithelial (mProx24) cells, both TM5275 and TM5441 effectively inhibited PAI-1-induced mRNA expression of fibrosis and inflammation markers and also reversed PAI-1-induced inhibition of plasmin activity, which confirmed the efficacy of the TM compounds as PAI-1 inhibitors. These data suggest that TM compounds could be used to prevent diabetic kidney injury.
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Registered trials
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