ArticleBiomedical reports2023
Pioglitazone modulates immune activation and ameliorates inflammation induced by injured renal tubular epithelial cells via PPARγ/miRNA‑124/STAT3 signaling.
Article in Biomedical reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Mechanism of claudin-2 in RTECs apoptosis after renal obstruction.Urolithiasis · 2026Article
- Modulatory effects of Pioglitazone on the CAF-driven malignant phenotype in cervical cancer: an in vitro bidirectional study.Discover oncology · 2026Article
- Combined dapagliflozin and pioglitazone therapy in diabetic nephropathy: no added benefit beyond monotherapy in inflammation and fibrosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Vitamin B12-Loaded Chitosan Nanoparticles Promote Skeletal Muscle Injury Repair in Aged Rats via Amelioration of Aging-Suppressed Efferocytosis.Biomolecules · 2025Article
- Anti-Obesity Properties ofMolecules (Basel, Switzerland) · 2025Article
- The role of microRNAs in nicotine signaling.EXCLI journal · 2023Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
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Abstract
Acute kidney injury (AKI) is commonly a result of renal ischemia reperfusion injury (IRI), which produces clinical complications characterized by the rapid deterioration of renal function, leading to chronic kidney disease and increases the risk of morbidity and mortality. Currently, only supportive treatment is available. AKI, which is accompanied by immune activation and inflammation, is caused by proximal tubular injury. The present study investigated the role of tubular epithelial cells as drivers of inflammation in renal IRI and their potential function as antigen-presenting cells, as well as the molecular mechanisms by which peroxisome proliferator-activated receptor-γ (PPARγ) agonists [such as pioglitazone (Pio)] exert reno-protective action in renal IRI. A total of 50 Wistar male albino rats were divided into five groups: Sham + DMSO, Sham + Pio, IRI + DMSO, IRI + prophylactic preoperative (pre) Pio and IRI + postoperative Pio. The histopathological changes in renal tissue samples and the renal epithelial cell expression of CD86, miRNA-124, STAT3, pro-inflammatory cytokines, inducible nitric oxide synthase (iNOS) and Arginase-II were analyzed by immunohistochemistry, reverse transcription-quantitative PCR, western blotting and ELISA respectively. IRI was a potent inducer for CD86 immunoexpression. An ameliorative action of Pio was demonstrated via decreased CD86 immunoexpression, upregulation of miRNA-124, decreased STAT3 expression and beneficial anti-inflammatory effects. The tubular epithelium served a notable role in the inflammatory response in renal IRI. Pio exerted its anti-inflammatory effects via PPARγ/miRNA-124/STAT3 signaling.
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