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Adipocyte-derived small extracellular vesicles exacerbate diabetic ischemic heart injury by promoting oxidative stress and mitochondrial-mediated cardiomyocyte apoptosis.
Redox Biol
December 2024
Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA, USA; Department of Biomedical Engineering, UAB, Birmingham, AL, USA. Electronic address:
Background: Diabetes increases ischemic heart injury via incompletely understood mechanisms. We recently reported that diabetic adipocytes-derived small extracellular vesicles (sEV) exacerbate myocardial reperfusion (MI/R) injury by promoting cardiomyocyte apoptosis. Combining in vitro mechanistic investigation and in vivo proof-concept demonstration, we determined the underlying molecular mechanism responsible for diabetic sEV-induced cardiomyocyte apoptosis after MI/R.
View Article and Find Full Text PDFCardiomyocyte-specific Piezo1 deficiency mitigates ischemia-reperfusion injury by preserving mitochondrial homeostasis.
Redox Biol
December 2024
Innovation Research Center, Shandong University of Traditional Chinese Medicine, Jinan, 250307, China; Lingnan Medical Research Center, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, 510260, China; School of Biomedical Sciences, Faculty of Biological Sciences, University of Leeds, LS2 9JT, UK. Electronic address:
Ca overload and mitochondrial dysfunction play crucial roles in myocardial ischemia-reperfusion (I/R) injury. Piezo1, a mechanosensitive cation channel, is essential for intracellular Ca homeostasis. The objective of this research was to explore the effects of Piezo1 on mitochondrial function during myocardial I/R injury.
View Article and Find Full Text PDFHydrogen gas inhalation therapy may not work sufficiently to mitigate oxidative stress induced with REBOA.
Sci Rep
December 2024
Department of Emergency and Critical Care Medicine, Jichi Medical University, Shimotsuke City, Tochigi, Japan.
Hemorrhagic shock is a significant cause of trauma-related mortality. Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a less-invasive aortic occlusion maneuver for severe hemorrhagic shock but potentially inducing oxidative stress injuries. In an animal model, this study investigated hydrogen gas inhalation therapy's potential to mitigate post-REBOA ischemia-reperfusion injuries (IRIs).
View Article and Find Full Text PDFmir-330-5p from mesenchymal stem cell-derived exosomes targets SETD7 to reduce inflammation in rats with cerebral ischemia-reperfusion injury.
J Mol Histol
December 2024
The Second Clinical Medical College, Southern Medical University, Guangzhou City, Guangdong Province, 510515, China.
This study was to investigate the role of microRNA (miR)-330-5p derived from mesenchymal stem cells-secreted exosomes (MSCs-Exo) in cerebral ischemia-reperfusion injury (CI/RI) through targeting lysine N-methyltransferase SET domain containing 7 (SETD7). MSCs-Exo were separated and identified. MSCs-Exo were used to treat the middle cerebral artery occlusion (MCAO) rat model.
View Article and Find Full Text PDFDeficiency of purinergic P2Y2 receptor impairs the recovery after renal ischemia-reperfusion injury and accelerates renal fibrosis and tubular senescence in mice.
Sci Rep
December 2024
Department of Pharmacology, Institute of Health Sciences, Gyeongsang National University College of Medicine, 15, 816 Beon-gil, Jinjudaero, Jinju, 52727, Republic of Korea.
Chronic kidney disease is defined as a progressive loss of kidney function associated with impaired recovery after acute kidney injury. Renal ischemia-reperfusion (IR) induces oxidative stress and inflammatory responses leading to severe tissue damage, where incomplete or maladaptive repair accelerates renal fibrosis and aging. To investigate the role of the purinergic P2Y2 receptor (P2Y2R) in these processes, we used P2Y2R knockout (KO) mice subjected to IR.
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