“TRP inflammation” relationship in cardiovascular system

Abstract

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.

TRPA1 inhibition ameliorates pressure overload-induced cardiac hypertrophy and fibrosis in mice

“…Similarly, TRPC1 knockout, in coordination with calcineurin/NFAT signaling, preserves heart structure and function in pressure overload mouse models [ 8 ]. Transient receptor potential ankyrin 1 (TRPA1), which belongs to the TRP channel superfamily, is an important target in oxidative stress and inflammatory diseases [ 9 , 10 ]. Inhibiting the TRPA1 channel has been shown to attenuate fibrosis and the inflammatory response in ocular fibroblasts [ 11 ].…”

Alterations to the middle cerebral artery of the hypertensive-arthritic rat model potentiates intracerebral hemorrhage

“…The direct effect of inflammatory insult on MCA function is observed in our RD CFA groups, as the MCAs did not contract significantly to high luminal pressure. Both the endothelium and vascular smooth muscle cell dysfunction may have occurred due to the trigger of physical and chemical stress signals (Numata, Takahashi & Inoue, 2015) and kinases such as NF-κB (Chauhan et al, 2014). The trigger may affect specific endothelial transient receptor potential (TRP) channels such as TRPV1 and TRPV4 with subsequent vasodilation (Kwan, Huang & Yao, 2007), thus impairing pressure-induced contractile response in RD CFAs while maintaining bradykinin’s endothelial response.…”

Roles of transient receptor potential channels in regulation of vascular and epithelial barriers

“…These aspects of TRP channel biology have been extensively reviewed. [72][73][74][75][76] In keeping with the theme of regulating barriers, here we will focus on the very small literature on the role of TRP channels in the migration of leukocytes across endothelial barriers. Neutrophils lacking TRPC6 do not migrate efficiently in response to CXCL2; 44 and TRPC6 was shown to be required for chemotaxis mediated by CXCR2 receptor signaling, but not that of N-formyL-methionine-leucine-phenylalanine (fMLF) receptor.…”