Results 121 to 130 of about 50,311 (298)

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

open access: yesThe 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   +5 more
wiley   +1 more source

Protection Against Cardiac Injury by Small Ca\u3csup\u3e2 +\u3c/sup\u3e-Sensitive K\u3csup\u3e+\u3c/sup\u3e Channels Identified in Guinea Pig Cardiac Inner Mitochondrial Membrane [PDF]

open access: yes, 2013
We tested if small conductance, Ca2 +‐sensitive K+ channels (SKCa) precondition hearts against ischemia reperfusion (IR) injury by improving mitochondrial (m) bioenergetics, if O2‐derived free radicals are required to initiate protection via SKCa ...
Aldakkak, Mohammed   +9 more
core   +1 more source

Serum from Patients Undergoing Remote Ischemic Preconditioning Protects Cultured Human Intestinal Cells from Hypoxia-Induced Damage: Involvement of Matrixmetalloproteinase-2 and -9 [PDF]

open access: gold, 2011
Karina Zitta   +8 more
openalex   +1 more source

The role of extracellular vesicles in cell–cell crosstalk in cardiotoxicity

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Administration of a pharmacological agent can result in off‐target cardiotoxicity which can be driven by cell–cell crosstalk between healthy and dysfunctional cardiac cells. Extracellular vesicles (EVs) are lipid bilayer structures that can move biological cargo between cells, facilitating cell–cell crosstalk.
Gabriella Bachynskyj‐Bilas   +5 more
wiley   +1 more source

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

open access: yesThe 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   +7 more
wiley   +1 more source

The challenge of translating ischemic conditioning from animal models to humans: the role of comorbidities

open access: yesDisease Models & Mechanisms, 2014
Following a period of ischemia (local restriction of blood supply to a tissue), the restoration of blood supply to the affected area causes significant tissue damage.
Kieran McCafferty   +3 more
doaj   +1 more source

HBO‐PC Reprograms Neuroimmune Metabolism Through Disruption of the LRG1‐HIF‐1α‐IL‐6‐STAT3 Amplification Loop Attenuates Pyroptosis and Ischemia–Reperfusion Injury

open access: yesCNS Neuroscience &Therapeutics, Volume 32, Issue 5, May 2026.
A mouse CIRI model was generated by middle cerebral artery occlusion. HBO‐PC and LRG1 siRNA knockdown were applied. Neurological function and molecular changes were evaluated. We confirmed that HBO‐PC reprograms neuroimmune metabolism through disruption of the LRG1‐HIF‐1α‐IL‐6‐STAT3 amplification Loop attenuates pyroptosis and ischemia–reperfusion ...
Wenying Lv   +5 more
wiley   +1 more source

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