ArticleAmerican journal of physiology. Renal physiology2016
Delayed treatment with PTBA analogs reduces postinjury renal fibrosis after kidney injury.
Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 34 citations in OpenAlex.
- Assays to measure small molecule Hsp70 agonist activity in vitro and in vivo.Analytical biochemistry · 2025Article
- Bibliometric and visualization analysis of kidney repair associated with acute kidney injury from 2002 to 2022.Frontiers in pharmacology · 2023Article
- From AKI to CKD: Maladaptive Repair and the Underlying Mechanisms.International journal of molecular sciences · 2022Review
- Experimental models of acute kidney injury for translational research.Nature reviews. Nephrology · 2022Review
- Kidney repair and regeneration: perspectives of the NIDDK (Re)Building a Kidney consortium.Kidney international · 2022Article
- Validation of HDAC8 Inhibitors as Drug Discovery Starting Points to Treat Acute Kidney Injury.ACS pharmacology & translational science · 2022Article
- Modeling oxidative injury response in human kidney organoids.Stem cell research & therapy · 2022Article
- Therapies Targeting Epigenetic Alterations in Acute Kidney Injury-to-Chronic Kidney Disease Transition.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Tubular Cell Cycle Response upon AKI: Revising Old and New Paradigms to Identify Novel Targets for CKD Prevention.International journal of molecular sciences · 2021Review
- Review
- Histone Deacetylases in Kidney Physiology and Acute Kidney Injury.Seminars in nephrology · 2020Review
- Time-dependent effects of histone deacetylase inhibition in sepsis-associated acute kidney injury.Intensive care medicine experimental · 2020Article
- Capillary rarefaction is more closely associated with CKD progression after cisplatin, rhabdomyolysis, and ischemia-reperfusion-induced AKI than renal fibrosis.American journal of physiology. Renal physiology · 2019Article
- Long-term outcomes in mouse models of ischemia-reperfusion-induced acute kidney injury.American journal of physiology. Renal physiology · 2019Article
- Cell-free hemoglobin augments acute kidney injury during experimental sepsis.American journal of physiology. Renal physiology · 2019Article
- Emerging strategies to disrupt the central TGF-β axis in kidney fibrosis.Translational research : the journal of laboratory and clinical medicine · 2019Review
- Enhancing regeneration after acute kidney injury by promoting cellular dedifferentiation in zebrafish.Disease models & mechanisms · 2019Article
- The role of macrophages during acute kidney injury: destruction and repair.Pediatric nephrology (Berlin, Germany) · 2019Review
- Review
- Translating Knowledge Into Therapy for Acute Kidney Injury.Seminars in nephrology · 2018Review
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
Abstract
No therapies have been shown to accelerate recovery or prevent fibrosis after acute kidney injury (AKI). In part, this is because most therapeutic candidates have to be given at the time of injury and the diagnosis of AKI is usually made too late for drugs to be efficacious. Strategies to enhance post-AKI repair represent an attractive approach to address this. Using a phenotypic screen in zebrafish, we identified 4-(phenylthio)butanoic acid (PTBA), which promotes proliferation of embryonic kidney progenitor cells (EKPCs), and the PTBA methyl ester UPHD25, which also increases postinjury repair in ischemia-reperfusion and aristolochic acid-induced AKI in mice. In these studies, a new panel of PTBA analogs was evaluated. Initial screening was performed in zebrafish EKPC assays followed by survival assays in a gentamicin-induced AKI larvae zebrafish model. Using this approach, we identified UPHD186, which in contrast to UPHD25, accelerates recovery and reduces fibrosis when administered several days after ischemia-reperfusion AKI and reduces fibrosis after unilateral ureteric obstruction in mice. UPHD25 and 186 are efficiently metabolized to the active analog PTBA in liver and kidney microsome assays, indicating both compounds may act as PTBA prodrugs in vivo. UPHD186 persists longer in the circulation than UPHD25, suggesting that sustained levels of UPHD186 may increase efficacy by acting as a reservoir for renal metabolism to PTBA. These findings validate use of zebrafish EKPC and AKI assays as a drug discovery strategy for molecules that reduce fibrosis in multiple AKI models and can be administered days after initiation of injury.
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Registered trials
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.