Hydrogen Sulfide Mitigates Myocardial Infarction via Promotion of Mitochondrial Biogenesis-Dependent M2 Polarization of Macrophages.

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  • Additional Information
    • Source:
      Publisher: Mary Ann Liebert, Inc Country of Publication: United States NLM ID: 100888899 Publication Model: Print Cited Medium: Internet ISSN: 1557-7716 (Electronic) Linking ISSN: 15230864 NLM ISO Abbreviation: Antioxid Redox Signal Subsets: MEDLINE
    • Publication Information:
      Original Publication: Larchmont, NY : Mary Ann Liebert, Inc., 1999-
    • Subject Terms:
      Organelle Biogenesis*; Hydrogen Sulfide/*pharmacology ; Macrophages/*drug effects ; Macrophages/*physiology ; Myocardial Infarction/*etiology ; Myocardial Infarction/*metabolism; Animals ; Disease Models, Animal ; Fatty Acids/metabolism ; Heart Function Tests ; Lipolysis ; Male ; Mice ; Mice, Knockout ; Monocytes/drug effects ; Monocytes/immunology ; Monocytes/metabolism ; Myocardial Infarction/diagnosis ; Myocardial Infarction/mortality ; Myocytes, Cardiac ; Oxidation-Reduction ; Ventricular Dysfunction/drug therapy
    • Abstract:
      Aims: Macrophages are of key importance for tissue repair after myocardial infarction (MI). Hydrogen sulfide (H2S) has been shown to exert cardioprotective effects in MI. However, the mechanisms by which H2S modulates cardiac remodeling and repair post-MI remain to be clarified.
      Results: In our current study, we showed that H2S supplementation ameliorated pathological remodeling and dysfunction post-MI in wild-type (WT) and CSE KO mice, resulting in decreased infarct size and mortality, accompanied by an increase in the number of M2-polarized macrophages at the early stage of MI. Strikingly, adoptive transfer of NaHS-treated bone marrow-derived macrophages into WT and CSE KO mice with depleted macrophages also ameliorated MI-induced cardiac functional deterioration. Further mechanistic studies demonstrated that NaHS-induced M2 polarization was achieved by enhanced mitochondrial biogenesis and fatty acid oxidation.
      Innovation and Conclusion: Our study shows (for the first time) that H2S may have the potential as a therapeutic agent for MI via promotion of M2 macrophage polarization. Rebound Track: This work was rejected during standard peer review and rescued by Rebound Peer Review (Antioxid Redox Signal 16:293-296, 2012) with the following serving as open reviewers: Hideo Kimura, Chaoshu Tang, Xiaoli Tian, and Kenneth Olson. Antioxid. Redox Signal. 25, 268-281.
    • Comments:
      Erratum in: Antioxid Redox Signal. 2023 Feb;38(4-6):461-462. (PMID: 36795005)
    • Grant Information:
      MR/M022706/1 United Kingdom MRC_ Medical Research Council
    • Accession Number:
      0 (Fatty Acids)
      YY9FVM7NSN (Hydrogen Sulfide)
    • Publication Date:
      Date Created: 20160615 Date Completed: 20170810 Latest Revision: 20230216
    • Publication Date:
      20240104
    • Accession Number:
      10.1089/ars.2015.6577
    • Accession Number:
      27296720