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Nitroxyl protects H9C2 cells from H/R-induced damage and inhibits autophagy via PI3K/Akt/mTOR pathway.
PLoS One
January 2025
Precision Laboratory of Vascular Medicine, Shanxi Cardiovascular Hospital Affiliated Shanxi Medical University, Taiyuan, PR China.
Background: Myocardial ischemia-reperfusion injury (MIRI) is an important complication in the treatment of heart failure, and its treatment has not made satisfactory progress. Nitroxyl (HNO) showed protective effects on the heart failure, however, the effect and underlying mechanism of HNO on MIRI remain largely unclear.
Methods: MIRI model in this study was established to induce H9C2 cell injury through hypoxia/reoxygenation (H/R) in vitro.
VEGFR3 mitigates hypertensive nephropathy by enhancing mitophagy via regulating crotonylation of HSPA1L.
Cell Commun Signal
January 2025
Department of Cardiology, the 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.
Oxidative stress-associated proximal tubular cells (PTCs) damage is an important pathogenesis of hypertensive renal injury. We previously reported the protective effect of VEGFR3 in salt-sensitive hypertension. However, the specific mechanism underlying the role of VEGFR3 in kidney during the overactivation of the renin-angiotensin-aldosterone system remains unclear.
View Article and Find Full Text PDFMitochondrial apoptosis in response to cardiac ischemia-reperfusion injury.
J Transl Med
January 2025
Department of Cardiovascular Ultrasound, The First Hospital of China Medical University, Shenyang, China.
In patients with acute myocardial infarction (AMI), thrombolytic therapy and revascularization strategies allow complete recanalization of occluded epicardial coronary arteries. However, approximately 35% of patients still experience myocardial ischemia/reperfusion (I/R) injury, which contributing to increased AMI mortality. Therefore, an accurate understanding of myocardial I/R injury is important for preventing and treating AMI.
View Article and Find Full Text PDFToll-Like Receptor 4-Mediated Neuroinflammation: Updates on Pathological Roles and Therapeutic Strategies in Chronic Cerebral Hypoperfusion.
Mol Neurobiol
January 2025
Department of Anatomy, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.
Neuroinflammation has been acknowledged as being one of the main pathologies that occur following chronic cerebral hypoperfusion (CCH). Since it significantly contributes to neuronal cell damage and thereby leads to cognitive impairment, the signals related to inflammation in hypoperfusion injury have been extensively investigated over the past few years. Toll-like receptor 4 (TLR4) is the key receptor responsible for immune and inflammatory reactions.
View Article and Find Full Text PDFEndovascular management of an aortic injury in thoracic kyphosis surgery: a minimally invasive rescue for a life-threatening injury.
BMJ Case Rep
January 2025
Department of Orthopaedics and Spine Surgery, Military Hospital Khadki, Pune, Maharashtra, India.
A patient in his early adolescence, who was treated for T5-T6 tubercular spondylodiscitis with an un-instrumented decompression, presented at 36 months post-index surgery, for post-laminectomy instability and kyphosis, after completing his requisite antitubercular treatment. He underwent thoracic posterior instrumented kyphosis correction and anterior reconstruction, with a T5-T6 partial corpectomy and corpectomy spacer placement, through a posterior midline incision. On the second postoperative day, he started complaining of pain on the left side of his chest, abdomen and left shoulder.
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