ArticleCell proliferation2022
TGF-β1 peptide-based inhibitor P144 ameliorates renal fibrosis after ischemia-reperfusion injury by modulating alternatively activated macrophages.
Article in Cell proliferation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- The Lactate-lactylation circuitry in kidney fibrosis: cellular crosstalk from tubular metabolic reprogramming to macrophage effector functions.Seminars in immunopathology · 2026Review
- Dynamic regulation and targeted interventions of macrophages in ischemia-reperfusion injury.Journal of advanced research · 2026Review
- Rubiadin-1-methyl ether alleviates bleomycin induced pulmonary fibrosis.Scientific reports · 2026Article
- Protecting kidney function: from mechanisms to therapeutic targets and traditional Chinese medicine.Renal failure · 2025Review
- Renoprotective Effects of MIT-001 in Ischemia-Reperfusion Injury: Modulation of Ferroptosis, ROS and Fibrotic Markers.Journal of cellular and molecular medicine · 2025Article
- Kurarinone protects against renal injury and fibrosis after unilateral ureteral obstruction through enhancement of the Nrf-2 signaling pathway.Journal of molecular histology · 2025Article
- JZL-184 Alleviate Neurological Impairment through Regulation of Mitochondrial Transfer and Lipid Droplet Accumulation after Cardiac Arrest.Molecular neurobiology · 2025Article
- Effects of Peptides and Bioactive Peptides on Acute Kidney Injury: A Review Study.Iranian biomedical journal · 2025Review
- Kidney Fibrosis In Vitro and In Vivo Models: Path Toward Physiologically Relevant Humanized Models.Advanced healthcare materials · 2025Review
- Leucine-rich alpha-2-glycoprotein 1 deficiency suppresses ischemia-reperfusion injury-induced renal fibrosis.Scientific reports · 2025Article
- Targeted Therapy for Skeletal Muscle Fibrosis: Regulation of Myostatin, TGF-β, MMP, and TIMP to Maintain Extracellular Matrix Homeostasis.Biologics : targets & therapy · 2025Review
- Depleting profibrotic macrophages using bioactivated in vivo assembly peptides ameliorates kidney fibrosis.Cellular & molecular immunology · 2024Article
- Emodin inhibits M1 macrophage activation that related to acute and chronic kidney injury through EGFR/MAPK pathway.Functional & integrative genomics · 2024Article
- Targeting Macrophages: Therapeutic Approaches in Diabetic Kidney Disease.International journal of molecular sciences · 2024Review
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- Pyruvate kinase M2 regulates kidney fibrosis through pericyte glycolysis during the progression from acute kidney injury to chronic kidney disease.Cell proliferation · 2024Article
- Macrophages polarization in renal inflammation and fibrosis animal models (Review).Molecular medicine reports · 2024Review
- The pathogenic role of succinate-SUCNR1: a critical function that induces renal fibrosis via M2 macrophage.Cell communication and signaling : CCS · 2024Article
- Taz/Tead1 Promotes Alternative Macrophage Activation and Kidney Fibrosis via Transcriptional Upregulation of Smad3.Journal of immunology research · 2024Article
- PDGFβ receptor-targeted delivery of truncated transforming growth factor β receptor type II for improving the in vitro and in vivo anti-renal fibrosis activity via strong inactivation of TGF-β1/Smad signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
objectivesIschemia-reperfusion injury (IRI) is a major cause of chronic renal fibrosis. Currently, numerous therapies have shown a minimal effect on the blockade of fibrosis progression. Here, the therapeutic potential of peptide-based TGF-β1 inhibitor P144 in IRI-induced renal fibrosis and the underlying mechanism were analyzed. MATERIALS AND
methodsThe unilateral ischemia-reperfusion injury with the contralateral nephrectomy model was established, and the P144 was administered intravenously 1d/14d after the onset of IRI. The histopathology and immunofluorescence staining were used to detect renal fibrosis and macrophage infiltration. The in vivo fluorescence imaging was used to measure the bio-distribution of P144. The transwell assays were used to observe the migration of macrophages. RT-qPCR and western blot were used to analyze TGF-β1 signaling.
resultsP144 ameliorated the accumulation of extracellular matrix in the kidney and improved the renal function in the unilateral ischemia-reperfusion injury plus contralateral nephrectomy model. Mechanistically, P144 downregulated the TGF-β1-Smad3 signaling at both the transcriptional and translational levels and further reduced the TGF-β1-dependent infiltration of macrophages to the injured kidney. Additionally, P144 blocked the polarization of macrophages to an M2-like phenotype induced by TGF-β1 in vitro, but showed no effect on their proliferation.
conclusionsOur study showed that the TGF-β1 peptide-based inhibitor P144 decreased renal fibrosis through the blockade of the TGF-β1-Smad3 signaling pathway and the modulation of macrophage polarization, suggesting its potential therapeutic use in IRI-induced renal fibrosis.
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