Results 111 to 120 of about 2,074,884 (292)
Activation of BNIP3-mediated mitophagy protects against renal ischemia–reperfusion injury
Acute kidney injury (AKI) is a syndrome of abrupt loss of renal functions. The underlying pathological mechanisms of AKI remain largely unknown. BCL2-interacting protein 3 (BNIP3) has dual functions of regulating cell death and mitophagy, but its ...
Chengyuan Tang +11 more
semanticscholar +1 more source
Norepinephrine/α2B‐adrenoceptor axis promotes the secretion of Notch2 intracellular domain (N2ICD)‐enriched extracellular vesicles (EVs) from macrophages. These EVs deliver N2ICD into fibroblasts, thereby inducing their activation. Deletion of Notch2 or α2B‐AR in macrophages disrupts N2ICD‐enriched EV formation and alleviates kidney fibrosis in mice ...
Huiwen Ren +14 more
wiley +1 more source
Cav3.2 channel regulates cerebral ischemia/reperfusion injury: a promising target for intervention
Calcium influx into neurons triggers neuronal death during cerebral ischemia/reperfusion injury. Various calcium channels are involved in cerebral ischemia/reperfusion injury. Cav3.2 channel is a main subtype of T-type calcium channels.
Feibiao Dai +9 more
doaj +1 more source
Total Thiols and MDA Levels in Patients with Acute Myocardial Infarction Before and After Reperfusion Therapy [PDF]
Background: Reactive oxygen species have been implicated in the pathogenesis of ischemic and reperfusion injury. In the current work we have measured malondialdehyde (MDA), total thiols, total CK, CK-MB and AST in ECG proven acute myocardial infarction ...
Babu, Suresh +2 more
core +1 more source
Ferroptosis is a recently identified form of regulated cell death defined by the iron-dependent accumulation of lipid reactive oxygen species. Ferroptosis has been studied in various diseases such as cancer, Parkinson’s disease, and stroke.
Yang Li +10 more
semanticscholar +1 more source
This work demonstrates that endothelial EphA4 limits Tie2 activation and curbs leptomeningeal collateral expansion after ischemic stroke. Pharmacological activation of Tie2 by an Ang‐1 mimetic or genetic loss of EphA4 stimulates collateral vessel growth, improves cerebral perfusion, and enhances neurological recovery.
Alexandra M. Kaloss +9 more
wiley +1 more source
A major goal in the treatment of acute ischemia of a vascular territory is to restore blood flow to normal values, i.e. to "reperfuse" the ischemic vascular bed.
Danielle G Souza, Mauro M Teixeira
doaj +1 more source
Pharmacologic modulation of experimental postischemic hepatic function [PDF]
The present study, evaluated and compared the effects of SRI 63-441, a potent platelet activating factor antagonist, superoxide dismutase (SOD), an oxygen free radical scavenger, and ibuprofen, a cyclooxygenase inhibitor on hepatic function after 90 ...
Makowka, L +5 more
core +2 more sources
FMO2 Promotes Angiogenesis via Regulation of N‐Acetylornithine
This study identifies flavin‐containing monooxygenase 2 (FMO2) as a novel proangiogenic regulator in endothelial cells. Targeted FMO2 ablation impairs vessel sprouting, whereas its compensation potently enhances angiogenesis. Metabolomics and single‐cell sequencing reveal that FMO2 drives vascular growth via the N‐acetylornithine/ATF3/NOTCH1 axis ...
Jingyi Wang +15 more
wiley +1 more source
The Role of Mitochondria in the Mechanisms of Cardiac Ischemia-Reperfusion Injury
Mitochondria play a critical role in maintaining cellular function by ATP production. They are also a source of reactive oxygen species (ROS) and proapoptotic factors.
A. Kuznetsov +5 more
semanticscholar +1 more source

