Hyperglycemia triggers RyR2-dependent alterations of mitochondrial calcium homeostasis in response to cardiac ischemia-reperfusion: Key role of DRP1 activation.
Stabilization of RyR2 maintains right ventricular function reduces the development of ventricular arrhythmias and improves prognosis in pulmonary hypertension.
Oxidative stress in early metabolic syndrome impairs cardiac RyR2 and SERCA2a activity and modifies the interplay of these proteins during Ca[2+] waves.
results provide preclinical experimental evidence that the cardiac expression of RyR2 nanobodies with AAV9 vectors is a promising therapeutic strategy for heart failure
Study shows that contextual fear memory formation and destabilization induce hippocampal ryanodine receptor (RyR2) calcium channel upregulation. The study proposes that both fear consolidation and extinction memories induce RyR2 protein upregulation in order to generate the intracellular Ca(2+) signals required for these distinct memory processes.
The present novel results emphasize the key role of redox-sensitive Ca(2+) release mediated by RyR2 channels for hippocampal structural plasticity and spatial memory.
RyR-2 regulated TGFbeta1 expression in mechanically stretched cardiomyocytes and TGFbeta1 promoted collagen formation of cardiac fibroblasts by a paracrine mechanism.
Data including data from studies in vesicles of knockout mice suggest pathophysiological levels of Zn2+ (>2nM) cause dysregulation of RyR2 opening; in sarcoplasmic reticulum RyR2 are not the only Ca2+-channels regulated by Zn2+; in cardiomyocytes exposed to ischemic/hypoxic conditions intracellular Zn2+ levels are elevated coinciding with increased MG23 expression. (RyR2 = ryanodine receptor 2; MG23 = mitsugumin 23)
RyR2-gated Ca(2+) store contributes to SOCE in pulmonary artery smooth muscle cells; however store-depletion alone is insufficient but requires a specific RyR conformation modifiable by ryanodine binding to activate Ca(2+) entry.
Results suggest that RyR2 play an important role in spinal cord injury through NOX2-mediated regulation of redox state and thus mitochondrial and ER dysfunction and inflammation as well.
HLP forms a triple complex with RyR2 and caveolin-3. siRNA and adenovirus-mediated KD of HLP decreased the electrically evoked Ca(2+) release from the sarcoplasmic reticulum
Data suggest that ryanodine receptor RyR2-mediated Ca2+ release induced by the concomitant increases in [Ca2+] and reactive oxygen species (ROS) produced by stimulatory glucose is an essential step in glucose-stimulated insulin secretion (GSIS).
Dual-tilt electron tomography showed cardiomyocyte and ventricular RYR2 tetramer packing within a dyad was nonuniform containing a mix of checkerboard and side-by-side arrangements as well as isolated tetramers.
An enhancement of antioxidant defence in diabetics via directly targeting heart seems to prevent diastolic dysfunction due to modulation of RyR2 macromolecular-complex thereby leading to normalized [Ca(2+)]i and [Zn(2+)]i in cardiomyocytes.
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