Showing papers in "Journal of Molecular and Cellular Cardiology in 2009"

TL;DR: In this paper, it was shown that the mitochondrial permeability transition pore (MPTP) is a major cause of reperfusion injury and an effective target for cardioprotection.

TL;DR: Using quantitative real-time RT-PCR, it is demonstrated that microRNA-21 (miR-21) was upregulated in cardiac myocytes after treatment with hydrogen peroxide (H(2)O(2)).

TL;DR: Evidence that TNFalpha can paradoxically initiate the activation of a novel protective pathway against reperfusion injuries is reviewed, which is named the Survivor Activating Factor Enhancement (SAFE) pathway, and its interaction with the RISK pathway is unravelled.

TL;DR: The role of free radicals in atherosclerosis is described and the mechanisms and cellular systems by which these radicals are produced are discussed and highlight recent technological advances which have added to the vascular biologist's armoury and promise to provide new insight into the role of reactive oxygen species in cardiovascular disease.

TL;DR: If is today considered as the most important ion channel involved in the rate regulation of cardiac pacemaker cells, and is sometimes referred to as “the pacemaker channel.” Several studies have shown that in addition to voltage and time, surface membrane electrogenic molecules are strongly modulated by Ca and phosphorylation.

TL;DR: The impact of pHi regulatory proteins on intracellular Ca2+ signalling, and their participation in clinical disorders such as myocardial ischaemia, maladaptive hypertrophy and heart failure emphasise the fundamental role that pHi regulation plays in the heart.

TL;DR: The findings, for the first time, established Nrf2 as a critical regulator of defense against ROS in normal and diabetic hearts.

TL;DR: Findings suggest that Notch1 signaling in aortic valve cells represses osteoblast-like calcification pathways mediated by Bmp2, which is part of a highly conserved signaling pathway involved in cell fate decisions, cell differentiation, and cardiac valve formation.

TL;DR: The results implicate PGC-1alpha and ERRalpha in the pathophysiology of human heart failure, and define dynamic target gene sets sharing known interrelated regulatory mechanisms capable of contributing to the mitochondrial dysfunction characteristic of this disease process.

TL;DR: These multifaceted activities of flavonoids raise their utility as possible therapeutic interventions to ameliorate ischemia-reperfusion injury.

TL;DR: The working hypothesis is that the occupied receptors migrate to caveolae, where signaling enzymes are scaffolded into signalosomes that bud off the plasma membrane and migrate to mitochondria, which initiates intramitochondrial signaling and inhibits the mitochondrial permeability transition (MPT), thus decreasing cell death.

TL;DR: The purpose of this review is to outline the current understanding of the molecular identity of the MPT pore and the many questions that still need to be answered.

TL;DR: This review will cover the recent field of mitochondrial dynamics and its physiological and pathological implications, with a particular emphasis on the experimental and theoretical basis of mitochondria dynamics in the heart.

TL;DR: The interaction between electrical and mechanical coupling is explored by reviewing studies performed in patients, animals, and in vitro and it is shown that impaired electrical coupling does not change mechanical coupling.

TL;DR: This review discusses recent findings shedding light on mechanisms by which titin elasticity is regulated dynamically and highlights novel links between titin and stress-signalling pathways in the cardiomyocyte.

TL;DR: Doxorubicin-induced cardiotoxicity is mediated by oxidative DNA damage-ATM-p53-apoptosis pathway, and is attenuated by pitavastatin through its antioxidant effect involving Rac1 inhibition.

TL;DR: The data suggest that JWH-133 administration during ischemia reduces the infarct size in a mouse model of myocardial ischemIA/reperfusion through a direct cardioprotective activity on cardiomyocytes and neutrophils.

TL;DR: Evidence is reviewed in support of the hypothesis that the wash-out of inhibitors or reversal of endogenous inhibition at reperfusion may afford protection by facilitating a more gradual wake-up of mitochondrial function, thereby avoiding a burst of ROS and Ca(2+) overload.

TL;DR: Fundamental differences in Ca(2+) homeostasis between atrial and ventricular cells are demonstrated and it is speculated that the increased SR Ca( 2+) content may be significant in determining the increased prevalence of arrhythmias in the atria.

TL;DR: The data demonstrate that SR-independent Ca(2+) transport mechanisms temporarily can prevent major cardiac dysfunction despite a major reduction of SERCA2 in cardiomyocytes.

TL;DR: Current knowledge regarding the role of NADPH oxidases in cardiomyocyte function in health and disease is reviewed.

TL;DR: This review summarizes the major factors involved in PTP control with specific emphasis on cardiovascular pathophysiology, and highlights recent findings on the pivotal role of inorganic phosphate as a mediator of the inhibitory effects of cyclosporin A and cyclophilin D ablation.

TL;DR: It is demonstrated that TB4 is the first known molecule capable of organ-wide activation of the embryonic coronary developmental program in the adult mammalian heart after systemic administration and that PKC plays a significant role in the process.

TL;DR: The current views on the role of inhibitor-1 in cardiac physiology, its possible contribution to cardiac disease and its potential as a novel therapeutic strategy are discussed.

TL;DR: A role of the mitochondrion as an integrator of calcium signalling and a fundamental decision maker in cardiomyocyte metabolism and survival is pointed to.

TL;DR: Interventions directed towards increasing plasma APN levels may improve endothelial function, and reduce cardiovascular complications suffered by diabetic patients, as well as investigate the involved mechanisms.

TL;DR: Real-time PCR data support a novel and previously unknown role for scleraxis in the regulation of collagen gene expression in the heart, including in post-infarct scar formation.

TL;DR: R/NIR light can decay nitrosyl hemes and release NO, and that this released NO may enhance the cardioprotective effects of nitrite, and the photodissociation to NO and its synergistic effect with sodium nitrite may represent a noninvasive and site specific means for increasing NO bioavailability.

TL;DR: The first BrS mutation in CaCNB2b is reported resulting in accelerated inactivation of L-type calcium channel current, suggesting that the faster current decay results in a loss of function responsible for the Brugada phenotype.

TL;DR: The use of genetically modified mouse models for studying cardiac biology is advocated and it is shown how, if employed properly, these models will continue to provide highly reliable data sets that suggest disease-gene relationships and novel therapeutic targets.