Results 241 to 250 of about 285,668 (333)

Research progress on the mechanisms related to myocardial injury in rats with myocardial ischemia-reperfusion injury treated by acupuncture at neiguan (PC6) acupoint: A narrative review. [PDF]

Medicine (Baltimore)
Xin Q, Gao Z, Guo J, Wang Y, Zhang Z, Liu Y, Yang B, Sun J.   +7 more
europepmc   +1 more source

Distinct profiles of mitochondrial bioenergetics and redox balance in left atrial and ventricular myocardium in the healthy rat heart

Experimental Physiology, EarlyView.
Abstract The left ventricle (LV) is the primary pumping chamber of the heart, generating high systolic pressure to sustain systemic circulation. LV contractile dysfunction is a hallmark of various cardiovascular diseases and is associated with mitochondrial dysfunction, characterised by decreased oxidative phosphorylation (OXPHOS) capacity and ...
Tingting Fang, Alex Chan, Janice Chew‐Harris, Toan Pham   +3 more
wiley   +1 more source

Glial cells in the heart: Implications for their roles in health and disease

The Journal of Physiology, EarlyView.
Abstract figure legend Schematic representation of cardiac autonomic ganglia within epicardial fat pads (posterior heart surface shown), containing vagal postganglionic neuron cell bodies, associated fibres, and glia. These ganglia receive cholinergic input from vagal preganglionic neurons and adrenergic input from sympathetic postganglionic neurons ...
Svetlana Mastitskaya, Rimma Dugarova, Shefeeq M. Theparambil   +2 more
wiley   +1 more source

Mitochondrial oxidative stress, calcium and dynamics in cardiac ischaemia‐reperfusion injury

The Journal of Physiology, EarlyView.
Abstract figure legend Heart attack causes ischaemia–reperfusion injury in cardiomyocytes. Mitochondria generate reactive oxygen species (ROS), leading to oxidative stress. High levels of mitochondrial calcium (Ca2+) activate the mitochondrial permeability transition pore (mPTP), and excess ROS levels can lower the Ca2+ required to activate the mPTP ...
Emily Rozich, Ulas Ozkurede, Shanmugasundaram Pakkiriswami, Ryan Gemilere, Samira M. Azarin, Julia C. Liu   +5 more
wiley   +1 more source

Inhibition of TREM1 attenuates myocardial ischemia-reperfusion injury-induced cardiomyocyte pyroptosis by suppressing the activation of the NF-κB signaling pathway. [PDF]

PLoS One
Xu X, Cai L, Dang X, Han J, Kou Y, Rong C, Kou J.   +6 more
europepmc   +1 more source

Targeting Myocardial Reperfusion Injury--The Search Continues.

New England Journal of Medicine, 2015
D. Hausenloy, D. Yellon
semanticscholar   +1 more source

Prediabetic cardiomyopathy is attenuated by hypothalamic PVN oxytocin neuron activation

The Journal of Physiology, EarlyView.
Abstract figure legend A long‐term high‐fat, high‐fructose diet induces prediabetes with insulin resistance, hyperinsulinaemia, elevated triglycerides and metabolic‐associated steatotic liver disease (MASLD) in male rats. Animals developed prediabetic cardiomyopathy characterized by diastolic dysfunction, interstitial fibrosis and tachycardia ...
Anna Nilsson, Joan Escobar, Kira Kuraoka, Ian Venter, Cielo A. Carnate, Matthew W. Kay, David Mendelowitz, Kathryn J. Schunke   +7 more
wiley   +1 more source

14‐3‐3 proteins: Regulators of cardiac excitation–contraction coupling and stress responses

The Journal of Physiology, EarlyView.
Abstract figure legend 14‐3‐3 protein interactions in cardiac regulation. Schematic representation of 14‐3‐3 binding partners in excitation–contraction coupling, transcriptional regulation/development and stress response pathways. Asterisks indicate targets where the exact 14‐3‐3 binding site is unknown.
Heather C. Spooner, Rose E. Dixon
wiley   +1 more source

The treatment of myocardial ischemia-reperfusion injury: potential roles of natural drug modulating CaMKII. [PDF]

Front Pharmacol
Yang K, Zhang P, Hui X, Liu C, Li J, Liu Y.   +5 more
europepmc   +1 more source

Small‐conductance Ca2⁺‐activated K⁺ channels in cardiac excitation–contraction coupling: Bridging mitochondria, sarcolemma and antiarrhythmic therapy

The Journal of Physiology, EarlyView.
Abstract figure legend Mitochondrial SK channel enhancement reduces cardiac arrhythmia trigger. Spontaneous sarcoplasmic reticulum (SR) Ca2+ release via hyperactive RyR2s underlies an increased arrhythmia trigger, promoting early and delayed afterdepolarizations during stress. Hyperactive RyR2s causes rise in cytosolic [Ca2+] during diastole. Clearance
Dmitry Terentyev, Alexey V. Glukhov, Vladimir Bogdanov, Aleksei S. Averin, Roland Veress, Bum‐Rak Choi, Shanna Hamilton, Andriy E. Belevych   +7 more
wiley   +1 more source