ArticleAmerican journal of physiology. Renal physiology2014
A PTBA small molecule enhances recovery and reduces postinjury fibrosis after aristolochic acid-induced kidney injury.
Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 76 citations in OpenAlex.
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Lactate metabolism and acute kidney injury.Chinese medical journal · 2025Review
- Epigenetic Regulation of Ferroptosis in Chronic Kidney Disease: Mechanisms and Implications.Research (Washington, D.C.) · 2025Review
- Review
- From Acute to Chronic: Unraveling the Pathophysiological Mechanisms of the Progression from Acute Kidney Injury to Acute Kidney Disease to Chronic Kidney Disease.International journal of molecular sciences · 2024Review
- Identification of histone deacetylase inhibitors as neutrophil recruitment modulators in zebrafish using a chemical library screen.Disease models & mechanisms · 2023Article
- Pretreatment with a novel Toll-like receptor 4 agonist attenuates renal ischemia-reperfusion injury.American journal of physiology. Renal physiology · 2023Article
- From AKI to CKD: Maladaptive Repair and the Underlying Mechanisms.International journal of molecular sciences · 2022Review
- Histone Deacetylases Cooperate with NF-κB to Support the Immediate Migratory Response after Zebrafish Pronephros Injury.International journal of molecular sciences · 2022Article
- Macrophage-derived, LRG1-enriched extracellular vesicles exacerbate aristolochic acid nephropathy in a TGFβR1-dependent manner.Cell biology and toxicology · 2022Article
- Experimental models of acute kidney injury for translational research.Nature reviews. Nephrology · 2022Review
- 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
- Preclinical and clinical progress for HDAC as a putative target for epigenetic remodeling and functionality of immune cells.International journal of biological sciences · 2021Review
- Epigenetics in kidney diseases.Advances in clinical chemistry · 2021Review
- The Role and Mechanism of Histone Deacetylases in Acute Kidney Injury.Frontiers in pharmacology · 2021Review
- Fractalkine (CX3CL1) and Its Receptor CX3CR1: A Promising Therapeutic Target in Chronic Kidney Disease?Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Phenylthiobutanoic acids (PTBAs) are a new class of histone deacetylase (HDAC) inhibitors that accelerate recovery and reduce postinjury fibrosis after ischemia-reperfusion-induced acute kidney injury. However, unlike the more common scenario in which patients present with protracted and less clearly defined onset of renal injury, this model of acute kidney injury gives rise to a clearly defined injury that begins to resolve over a short period of time. In these studies, we show for the first time that treatment with the PTBA analog methyl-4-(phenylthio)butanoate (M4PTB) accelerates recovery and reduces postinjury fibrosis in a progressive model of acute kidney injury and renal fibrosis that occurs after aristolochic acid injection in mice. These effects are apparent when M4PTB treatment is delayed 4 days after the initiating injury and are associated with increased proliferation and decreased G2/M arrest of regenerating renal tubular epithelial cells. In addition, there is reduced peritubular macrophage infiltration and decreased expression of the macrophage chemokines CX3Cl1 and CCL2. Since macrophage infiltration plays a role in promoting kidney injury, and since renal tubular epithelial cells show defective repair and a marked increase in maladaptive G2/M arrest after aristolochic acid injury, these findings suggest M4PTB may be particularly beneficial in reducing injury and enhancing intrinsic cellular repair even when administered days after aristolochic acid ingestion.
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Registered trials
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