期刊
ANTIOXIDANTS & REDOX SIGNALING
卷 25, 期 5, 页码 268-281出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2015.6577
关键词
-
资金
- National Nature Science Foundation of China [81330080]
- Shanghai Committee of Science and Technology in China [14JC1401100]
- Medical Research Council [MR/M022706/1] Funding Source: researchfish
- MRC [MR/M022706/1] Funding Source: UKRI
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 H(2)SZ 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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据