Results 141 to 150 of about 4,202 (274)

Insights from animal models: Dissecting the independent roles of oxygen and nutrients in the fetal origins of cardiovascular disease

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend This review utilized animal models of complicated human pregnancies that result in reduced fetal nutrient or oxygen delivery, or combined nutrient and oxygen delivery, to elucidate their independent and/or synergistic contributions to the development of high‐risk cardiac phenotypes.
Melanie R. Bertossa   +8 more
wiley   +1 more source

Hypertrophic cardiomyopathy mutations Y115H and E497D disrupt the folded-back state of human β-cardiac myosin allosterically. [PDF]

open access: yesNat Commun
Nandwani N   +9 more
europepmc   +1 more source

Demonstration of beat‐to‐beat, on‐demand ATP synthesis in ventricular myocytes reveals sex‐specific mitochondrial and cytosolic dynamics

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Beat‐locked mitochondrial ATP transients reveal modular, sex‐specific bioenergetic control during excitation–contraction coupling. A, each action potential activates L‐type CaV1.2 channels, producing a Ca2+ influx that triggers ryanodine receptors (RyR2) and elicits SR Ca2+ release.
Paula Rhana   +2 more
wiley   +1 more source

Cardiac Myosin Heavy Chains

open access: yesCardiology and Angiology: An International Journal, 2019
Muhanad S. Abdelwahab   +4 more
openaire   +1 more source

Human‐derived cardiac‐neural microtissues reveal catecholaminergic polymorphic ventricular tachycardia is also a disease of the sympathetic neuron

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend Schematic diagram illustrating the proposed pathway in which regulatory defects might occur in sympathetic neurons derived from hiPSC in catecholaminergic polymorphic ventricular tachycardia (CPVT). Specifically, enhanced calcium transients appeared to derive from three sources: enhanced membrane excitability (due to loss of ...
Ni Li   +19 more
wiley   +1 more source

Pulmonary parenchyma becomes a self-organized dissipative structure in lung cancers and pulmonary inflammatory diseases. [PDF]

open access: yesPhysiol Rep
Lecarpentier Y   +7 more
europepmc   +1 more source

Translating cardiovascular ion channel and Ca2+ signalling mechanisms into therapeutic insights

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend This white paper integrates mechanistic discoveries across ion channel biology, Ca2+ signalling and multiscale cardiovascular physiology to highlight new opportunities for accelerating research and guiding next‐generation therapies. Printed with permission from ®Anita Impagliazzo Medical Illustration. [Correction added on 2 March
Silvia Marchianò   +18 more
wiley   +1 more source

Exercise training prior to and during cancer in mice preserves muscle mass, reduces tumour weight and suppresses molecular mediators of cachexia

open access: yesThe Journal of Physiology, EarlyView.
Abstract figure legend PoWeR training (11.5 weeks of voluntary wheel running with progressively increased resistance) before and during cancer attenuates muscle loss, limits tumour growth, drives a transition toward a more oxidative muscle phenotype (IIB‐to‐IIA shift), downregulates cachexia‐associated pathways and enhances mitochondrial performance in
Stavroula Tsitkanou   +13 more
wiley   +1 more source

Home - About - Disclaimer - Privacy