Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The transient receptor potential (TRP) family of ion channels comprises more than 50 cation-permeable channels expressed throughout the animal kingdom. TRPs can be grouped into 7 main subfamilies according to structural homology: the TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPP (polycystin), TRPML (mucolipin), TRPA (ankyrin), and TRPN (NO mechanopotential). During the past 20 years, the cloning and characterization after reexpression of most members of these cation channels have led to a plethora of data and more recently to some understanding of their roles in various cells and tissues. Specifically in the heart, TRPs are known to be involved in various diseases, including hypertrophy, heart failure, and arrhythmia. The later part of this review focuses on the potential contribution of TRPs to cardiac rhythm and their potential proarrhythmic effects. Furthermore, several neurotransmitters that activate the formation of diacylglycerol could modulate cardiac rhythm or, like ATP, induce arrhythmia.
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PMID:Transient receptor potential: a large family of new channels of which several are involved in cardiac arrhythmia. 1923 73

Transient receptor potential (TRP) channels are expressed in almost every human tissue, including the heart and the vasculature. They play unique roles not only in physiological functions but, if over-expressed, also in pathophysiological disease states. Cardiovascular diseases are the leading cause of death in the industrialized countries. Therefore, TRP channels are attractive drug targets for more effective pharmacological treatments of these diseases. This review focuses on three major cell types of the cardiovascular system: cardiomyocytes as well as smooth muscle cells and endothelial cells from the systemic and pulmonary circulation. TRP channels initiate multiple signals in all three cell types (e.g. contraction, migration) and are involved in gene transcription leading to cell proliferation or cell death. Identification of their genes has significantly improved our knowledge of multiple signal transduction pathways in these cells. Some TRP channels are important cellular sensors and are mostly permeable to Ca(2+), while most other TRP channels are receptor activated and allow for the entry of Na(+), Ca(2+) and Mg(2+). Physiological functions of TRPA, TRPC, TRPM, TRPP and TRPV channels in the cardiovascular system, dissected by down-regulating channel activity in isolated tissues or by the analysis of gene-deficient mouse models, are reviewed. The involvement of TRPs as homomeric or heteromeric channels in pathophysiological processes in the cardiovascular system like heart failure, cardiac hypertrophy, hypertension as well as edema formation by increased endothelial permeability will be discussed.
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PMID:TRP channels in the cardiopulmonary vasculature. 2129 Mar 27

Calcium is an important second messenger required not only for the excitation-contraction coupling of the heart but also critical for the activation of cell signaling pathways involved in the adverse cardiac remodeling and consequently for the heart failure. Sustained neurohumoral activation, pressure-overload, or myocardial injury can cause pathologic hypertrophic growth of the heart followed by interstitial fibrosis. The consequent heart's structural and molecular adaptation might elevate the risk of developing heart failure and malignant arrhythmia. Compelling evidences have demonstrated that Ca²⁺ entry through TRP channels might play pivotal roles in cardiac function and pathology. TRP proteins are classified into six subfamilies: TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPA (ankyrin), TRPML (mucolipin), and TRPP (polycystin), which are activated by numerous physical and/or chemical stimuli. TRP channels participate to the handling of the intracellular Ca²⁺ concentration in cardiac myocytes and are mediators of different cardiovascular alterations. This review provides an overview of the current knowledge of TRP proteins implication in the pathologic process of some frequent cardiac diseases associated with the adverse cardiac remodeling such as cardiac hypertrophy, fibrosis, and conduction alteration.
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PMID:TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling. 3088 10

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