Results 121 to 130 of about 28,867 (291)

Calciprotein particle‐induced calcium overload triggers mitochondrial dysfunction in endothelial cells

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Calciprotein particles (CPPs) are small calcium‐ and phosphate‐containing nanoaggregates associated with the development of vascular disease (CVD) in chronic kidney disease (CKD). Previously, we have shown that CPPs induce endothelial cell (EC) dysfunction, possibly contributing to CVD in CKD, but the underlying molecular ...
Lian Feenstra   +9 more
wiley   +1 more source

Mechanisms altering airway smooth muscle cell Ca(2+) homeostasis in two asthma models [PDF]

open access: yes, 2008
Background: Asthma is characterized by airway remodeling, altered mucus production and airway smooth muscle cell (ASMC) contraction causing extensive airway narrowing. In particular, alterations of ASMC contractility seem to be of crucial importance. The
Bergner, Albrecht   +6 more
core   +1 more source

Intramuscular pathways of maladaptation in overtraining syndrome

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend The transition from adaptive overreaching to maladaptive overtraining and mechanisms through which excessive training load can lead to performance decline. Four interconnected pathophysiological domains are highlighted: neural fatigue, involving both central and peripheral components such as altered sensory feedback and reflex ...
Emily Shorter   +4 more
wiley   +1 more source

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

Mechanisms underlying local Ca2+ signalling differences between right and left atrial myocytes at normal and increased frequencies

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Left atrial myocytes have TAT‐associated faster Ca2+ release but are more prone to maladaptation at higher frequencies due to weaker peripheral SR Ca2+ uptake and smaller trigger Ca2+ current. Abstract Changes in heart rate affect Ca2+ signalling and contractility in ventricular muscle, but the effects on atrial Ca2+ signalling ...
Joon‐Chul Kim   +6 more
wiley   +1 more source

Catecholaminergic polymorphic ventricular tachycardia–linked ryanodine receptor variants exhibit domain‐specific calcium leak and calmodulin affinity properties

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Catecholaminergic polymorphic ventricular tachycardia (CPVT) variants in N terminal (NTD) and central domain (CD) but not pore domain induce a pathological RyR2 conformational shift upon protein kinase A (PKA) phosphorylation, similar to that seen in heart failure (HF), calcium/calmodulin‐dependent protein kinase II (CaMKII ...
Hitoshi Uchinoumi   +11 more
wiley   +1 more source

Inhibition of the skeletal muscle ryanodine receptor calcium release channel by nitric oxide

open access: yesFEBS Letters, 1996
NO donors were found to reduce the rate of Ca2+ release from isolated skeletal muscle sarcoplasmic reticulum (SR) and the open probability of single ryanodine receptor Ca2+ release channels (RyRCs) in planar lipid bilayers, and these effects were prevented by the NO quencher hemoglobin and reversed by 2‐mercaptoethanol.
Mészáros, LászlóG.   +2 more
openaire   +2 more sources

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

open access: yesThe 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

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