ArticleBioMed research international2020
HO-1/PINK1 Regulated Mitochondrial Fusion/Fission to Inhibit Pyroptosis and Attenuate Septic Acute Kidney Injury.
Article in BioMed research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Ergosterol alleviates lipopolysaccharide-induced acute kidney injury in rats via a mechanistic modulation of TLR4/p-p38/NF-κB, iNOS/NO and Nrf2/HO-1 signaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Mitochondrial calcium uniporter-mediated mitochondrial dynamics imbalance contributes to contrast medium-induced renal tubular cell injury.Frontiers in molecular biosciences · 2026Article
- Cobalt Protoporphyrin Downregulates Hyperglycemia-Induced Inflammation and Enhances Mitochondrial Respiration in Retinal Pigment Epithelial Cells.Antioxidants (Basel, Switzerland) · 2025Article
- Pyroptosis: The Determinator of Cell Death and Fate in Acute Kidney Injury.Kidney diseases (Basel, Switzerland) · 2024Review
- Retracted: HO-1/PINK1 Regulated Mitochondrial Fusion/Fission to Inhibit Pyroptosis and Attenuate Septic Acute Kidney Injury.BioMed research international · 2024Article
- The Role of Pyroptosis in the Pathogenesis of Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2023Review
- The Pharmacological Effect of Hemin in Inflammatory-Related Diseases: Protocol for a Systematic Review.JMIR research protocols · 2023Article
- Cytoprotective Role of Heme Oxygenase-1 in Cancer Chemoresistance: Focus on Antioxidant, Antiapoptotic, and Pro-Autophagy Properties.Antioxidants (Basel, Switzerland) · 2023Review
- Heme oxygenase‑1 inhibits renal tubular epithelial cell pyroptosis by regulating mitochondrial function through PINK1.Experimental and therapeutic medicine · 2023Article
- The Mitochondrion: A Promising Target for Kidney Disease.Pharmaceutics · 2023Review
- Blockage of S100A8/A9 ameliorates septic nephropathy in mice.Frontiers in pharmacology · 2023Article
- BACH1-Hemoxygenase-1 axis regulates cellular energetics and survival following sepsis.Free radical biology & medicine · 2022Article
- The critical role of ferritinophagy in human disease.Frontiers in pharmacology · 2022Review
- Levosimendan in rats decreases acute kidney injury after cardiopulmonary resuscitation by improving mitochondrial dysfunction.Translational andrology and urology · 2021Article
- Review
- The Programmed Cell Death of Macrophages, Endothelial Cells, and Tubular Epithelial Cells in Sepsis-AKI.Frontiers in medicine · 2021Review
- Mitofusin-2: A New Mediator of Pathological Cell Proliferation.Frontiers in cell and developmental biology · 2021Review
- Intracellular and Extracellular Lipopolysaccharide Signaling in Sepsis: Avenues for Novel Therapeutic Strategies.Journal of innate immunity · 2021Review
Corrections and comments
- Retraction · 2024-03-20Computer-Aided Content or Computer-Generated Content · Concerns/Issues about Data · Concerns/Issues about Referencing/Attributions · Concerns/Issues about Results and/or Conclusions · Concerns/Issues about Peer Review · Investigation by Journal/Publisher · Investigation by Third Party · Paper Mill · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEndotoxin-associated acute kidney injury (AKI), a disease characterized by marked oxidative stress and inflammation disease, is a major cause of mortality in critically ill patients. Mitochondrial fission and pyroptosis often occur in AKI. However, the underlying biological pathways involved in endotoxin AKI remain poorly understood, especially those related to mitochondrial dynamics equilibrium disregulation and pyroptosis. Previous studies suggest that heme oxygenase- (HO-) 1 confers cytoprotection against AKI during endotoxic shock, and PTEN-induced putative kinase 1 (PINK1) takes part in mitochondrial dysfunction. Thus, in this study, we examine the roles of HO-1/PINK1 in maintaining the dynamic process of mitochondrial fusion/fission to inhibit pyroptosis and mitigate acute kidney injury in rats exposed to endotoxin.
methodsAn endotoxin-associated AKI model induced by lipopolysaccharide (LPS) was used in our study. Wild-type (WT) rats and PINK1 knockout (PINK1KO) rats, respectively, were divided into four groups: the control, LPS, Znpp+LPS, and Hemin+LPS groups. Rats were sacrificed 6 h after intraperitoneal injecting LPS to assess renal function, oxidative stress, and inflammation by plasma. Mitochondrial dynamics, morphology, and pyroptosis were evaluated by histological examinations.
resultsIn the rats with LPS-induced endotoxemia, the expression of HO-1 and PINK1 were upregulated at both mRNA and protein levels. These rats also exhibited inflammatory response, oxidative stress, mitochondrial fission, pyroptosis, and decreased renal function. After upregulating HO-1 in normal rats, pyroptosis was inhibited; mitochondrial fission and inflammatory response to oxidative stress were decreased; and the renal function was improved. The effects were reversed by adding Znpp (a type of HO-1 inhibitor). Finally, after PINK1 knockout, there is no statistical difference in the LPS-treated group and Hemin or Znpp pretreated group.
conclusionsHO-1 inhibits inflammation response and oxidative stress and regulates mitochondria fusion/fission to inhibit pyroptosis, which can alleviate endotoxin-induced AKI by PINK1.
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