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MGST1 overexpression ameliorates mitochondrial dysfunction and ferroptosis during myocardial ischemia/reperfusion injury after heart transplantation.
Int J Biol Macromol
January 2025
Department of Thoracic Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China. Electronic address:
Mitochondrial dysfunction and ferroptosis play crucial roles in myocardial ischemia/reperfusion (I/R) following heart transplantation. Microsomal glutathione s transferase 1 (MGST1) is widely distributed in mitochondria and has a protective effect against ferroptosis, and its involvement in myocardial I/R injury has not yet been elucidated. In this study, donor hearts from C57BL/6 male mice were subjected to 12 h of ex-vivo cold ischemia treatment and transplanted into the abdomen of recipient mice for 24 h of reperfusion.
View Article and Find Full Text PDFSS-31@Fer-1 Alleviates ferroptosis in hypoxia/reoxygenation cardiomyocytes via mitochondrial targeting.
Biomed Pharmacother
January 2025
Department of Cardiology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China. Electronic address:
Purpose: Targeting mitochondrial ferroptosis presents a promising strategy for mitigating myocardial ischemia-reperfusion (I/R) injury. This study aims to evaluate the efficacy of the mitochondrial-targeted ferroptosis inhibitor SS-31@Fer-1 (elamipretide@ferrostatin1) in reducing myocardial I/R injury.
Methods: SS-31@Fer-1 was synthesized and applied to H9C2 cells subjected to hypoxia/reoxygenation (H/R) to assess its protective effects.
A novel Sai-based antioxidant agent attenuates antibody-mediated rejection in allogeneic rat kidney transplantation.
Am J Transplant
January 2025
Department of Urology, Osaka University Graduate School of Medicine, Suita, Japan; Department of Urology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan. Electronic address:
Antibody-mediated rejection (ABMR) remains a leading cause of graft loss during kidney transplantation. Ischemia reperfusion injury (IRI) has been reported to promote T-cell proliferation, leading to B-cell activation and subsequent production of donor-specific antibodies (DSA), which target antigens on the vascular endothelium. We hypothesize that a novel therapeutic strategy targeting highly toxic reactive oxygen species could mitigate oxidative stress and immune responses associated with IRI.
View Article and Find Full Text PDFMogroside V ameliorates astrocyte inflammation induced by cerebral ischemia through suppressing TLR4/TRADD pathway.
Int Immunopharmacol
January 2025
Medical College of Guangxi University, Guangxi University, Nanning 530004, China; Fujian Maternity and Child Health Hospital, Fuzhou, 350001, China; Stem Cell Therapy Research Center, Fuzhou 350001, China.. Electronic address:
Inflammation and oxidative stress are pivotal factors in the onset and progression of secondary injury following cerebral ischemia-reperfusion (I/R). Mogroside V (MV), a primary active compound of Siraitia grosvenorii, exhibits significant anti-inflammatory and antioxidant properties. However, its specific effects in cerebral ischemia remain unclear.
View Article and Find Full Text PDFConstruction of an lncRNA-mediated ceRNA network to investigate the inflammatory regulatory mechanisms of ischemic stroke.
PLoS One
January 2025
Department of Biochemistry, College of Medicine, Shihezi University, Shihezi, Xinjiang, China.
Long non-coding RNAs (lncRNAs) are among the most abundant types of non-coding RNAs in the genome and exhibit particularly high expression levels in the brain, where they play crucial roles in various neurophysiological and neuropathological processes. Although ischemic stroke is a complex multifactorial disease, the involvement of brain-derived lncRNAs in its intricate regulatory networks remains inadequately understood. In this study, we established a cerebral ischemia-reperfusion injury model using middle cerebral artery occlusion (MCAO) in male Sprague-Dawley rats.
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