Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Myocardial ischemia-reperfusion injury (MIRI) is a common clinic scenario that occurs in the context of reperfusion therapy for acute myocardial infarction. It has been shown that cocaine and amphetamine-regulated transcript (CART) can ameliorate cerebral ischemia-reperfusion (I/R) injury, but the effect of CART on MIRI has not been studied yet. Here, we revealed that CART protected the heart during I/R process by inhibiting apoptosis and excessive autophagy, indicating that CART would be a potential drug candidate for the treatment of MIRI. Further analysis showed that CART upregulated the activation of phospho-AKT, leading to downregulation of lactate dehydrogenase (LDH) release, apoptosis, oxidative stress and excessive autophagy after I/R, which was inhibited by PI3K inhibitor, LY294002. Collectively, CART attenuated MIRI through inhibition of cardiomyocytes apoptosis and excessive autophagy, and the protective effect was dependent on PI3K/AKT signalling pathway.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/1440-1681.13904 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Mitochondrial dysfunction in diabetic ulcers: pathophysiological mechanisms and targeted therapeutic strategies.
Front Cell Dev Biol
August 2025
Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Southwest Medical University, Luzhou, China.
Diabetic foot ulcers (DFUs) are a serious complication of diabetes, characterized by delayed wound healing, recurrent infection, and risk of amputation. Mitochondrial dysfunction has emerged as a central pathological mechanism underlying impaired wound healing. Persistent hyperglycemia triggers a cascade of mitochondrial abnormalities like disrupted calcium homeostasis, excessive ROS production, impaired autophagy, increased apoptosis, and imbalanced mitochondrial dynamics.
View Article and Find Full Text PDFExcess copper exposure and male reproductive toxicity: molecular mechanisms and potential interventions.
Biometals
September 2025
College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, 611130, Sichuan, People's Republic of China.
Copper (Cu) is an essential micronutrient in various enzymatic and physiological functions. However, excessive copper intake, mainly resulting from industrial emissions and improper agricultural practices, has raised growing concerns due to its toxicological effects, particularly on the male reproductive system. This review summarizes current research progress on copper-induced reproductive toxicity in males, emphasizing its impact on sperm quality, androgen production, and testicular structure and function.
View Article and Find Full Text PDFTXNIP promotes ferroptosis through NCOA4 mediated ferritinophagy.
Biochim Biophys Acta Mol Cell Res
September 2025
Department of Physiology and Pathophysiology, University of Manitoba, Health Sciences Centre, Winnipeg, Canada. Electronic address:
Ferroptosis is a recently discovered lytic form of cell death that is triggered by iron-driven excessive lipid peroxidation and depletion of glutathione and glutathione peroxidase-4 (GPX4). This form of cell death has been linked to a wide range of conditions from cancer to neurodegenerative diseases. Using murine hippocampal HT22 neurons, we aimed to investigate the underlying mechanisms of glutamate-mediated ferroptosis.
View Article and Find Full Text PDFEffects of Geniposide on Cerebral Ischemia/Reperfusion-Induced Neuron Damage by Inhibiting Autophagy via cGAS-STING.
Neuropharmacology
September 2025
College of Pharmacy, Shanghai University of Medicine and Health Sciences, Shanghai, China. Electronic address:
Aim Of The Study: This study aimed to investigate the protective effects of Geniposide (GEN) against cerebral ischemia-reperfusion injury by targeting the cGAS-STING pathway and modulating autophagy in neuronal cells.
Materials And Methods: In vivo middle cerebral artery occlusion/reperfusion (MCAO/R) model and an in vitro oxygen-glucose deprivation/reperfusion (OGD/R) model to mimic the pathology of cerebral ischemic stroke in humans. Behavioral tests, tissue staining to assess neurological deficits and tissue damage in mice.
The Role of P62/Nrf2/Keap1 Signaling Pathway in Lead-Induced Neurological Dysfunction.
CNS Neurosci Ther
September 2025
School of Public Health, Guangxi Medical University, Nanning, Guangxi, China.
Background: Lead (Pb) exposure is recognized for its contribution to the development of neurodegenerative diseases. However, the precise mechanisms underlying Pb-induced neurological dysfunction remain elusive. This study aimed to investigate the role of oxidative stress and the autophagy-related P62/kelch like ECH-associated protein 1 (Keap1)/Nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in neuronal impairment caused by Pb.
View Article and Find Full Text PDF