"TRP inflammation" relationship in cardiovascular system.
Despite considerable advances in the research and treatment, the precise relationship between inflammation and cardiovascular (CV) disease remains incompletely understood. Therefore, understanding the immunoinflammatory processes underlying the initiation, progression, and exacerbation of many cardiovascular diseases is of prime importance. The innate immune system has an ancient origin and is well conserved across species. Its activation occurs in response to pathogens or tissue injury. Recent studies suggest that altered ionic balance, and production of noxious gaseous mediators link to immune and inflammatory responses with altered ion channel expression and function. Among plausible candidates for this are transient receptor potential (TRP) channels that function as polymodal sensors and scaffolding proteins involved in many physiological and pathological processes. In this review, we will first focus on the relevance of TRP channel to both exogenous and endogenous factors related to innate immune response and transcription factors related to sustained inflammatory status. The emerging role of inflammasome to regulate innate immunity and its possible connection to TRP channels will also be discussed. Secondly, we will discuss about the linkage of TRP channels to inflammatory CV diseases, from a viewpoint of inflammation in a general sense which is not restricted to the innate immunity. These knowledge may serve to provide new insights into the pathogenesis of various inflammatory CV diseases and their novel therapeutic strategies.
Department of Physiology, Graduate School of Medical Sciences, Fukuoka University, Nanakuma 7-45-1, Johnan-ku, Fukuoka, 814-0180, Japan. numata@fukuoka-u.ac.jp.
Tomohiro
T
Numata
Department of Physiology, Graduate School of Medical Sciences, Fukuoka University, Nanakuma 7-45-1, Johnan-ku, Fukuoka, 814-0180, Japan.
Kiriko
K
Takahashi
Department of Physiology, Graduate School of Medical Sciences, Fukuoka University, Nanakuma 7-45-1, Johnan-ku, Fukuoka, 814-0180, Japan. inouery@fukuoka-u.ac.jp.
Ryuji
R
Inoue
D000818:Animals; D002318:Cardiovascular Diseases / Q000209:etiology / Q000378:metabolism; D002319:Cardiovascular System / Q000276:immunology / Q000378:metabolism*; D004198:Disease Susceptibility; D054884:Host-Pathogen Interactions; D006801:Humans; D007113:Immunity, Innate; D056747:Immunomodulation; D058847:Inflammasomes / Q000378:metabolism; D007249:Inflammation / Q000209:etiology* / Q000378:metabolism*; D018836:Inflammation Mediators / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction; D050051:Transient Receptor Potential Channels / Q000235:genetics* / Q000378:metabolism*
D058847:Inflammasomes; D018836:Inflammation Mediators; D017382:Reactive Oxygen Species; D050051:Transient Receptor Potential Channels
Cardiovascular; Disease; Inflammasome; Inflammation; Innate immune system; TRP