2017
DOI: 10.3389/fcvm.2017.00056
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Abstract: Cardiac stiffness, caused by interstitial fibrosis due to deposition of extracellular matrix proteins, is thought as a major clinical outcome of heart failure with preserved ejection fraction (HFpEF). Canonical transient receptor potential (TRPC) subfamily proteins are components of Ca2+-permeable non-selective cation channels activated by receptor stimulation and mechanical stress, and have been attracted attention as a key mediator of maladaptive cardiac remodeling. How TRPC-mediated local Ca2+ influx encode… Show more

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Cited by 34 publications
(30 citation statements)
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“…In addition, transgenic mice displayed no apparent changes in cardiac structure and function (Supplement 1C, 1D). This result confirmed that despite the influence of the high-Hcy diet and the TAC surgery, the protein level of TRPC3 and the related TGF-ß signalling pathway [9] were inhibited in the TRPC3-KD+HH group, while SIRT1 was increased. Similar results were observed in the SIRT1-overexpression+HH group with the higher level of SIRT1 ( Fig.…”
Section: Sirt1-overexpression and Trpc3-kd Mice Can Efficientlysupporting
confidence: 77%
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“…In addition, transgenic mice displayed no apparent changes in cardiac structure and function (Supplement 1C, 1D). This result confirmed that despite the influence of the high-Hcy diet and the TAC surgery, the protein level of TRPC3 and the related TGF-ß signalling pathway [9] were inhibited in the TRPC3-KD+HH group, while SIRT1 was increased. Similar results were observed in the SIRT1-overexpression+HH group with the higher level of SIRT1 ( Fig.…”
Section: Sirt1-overexpression and Trpc3-kd Mice Can Efficientlysupporting
confidence: 77%
“…Although TRPC3 is well established to play a central role in transducing cardiac fibrosis signalling [21] , the mechanisms underlying its signal transduction function still remain poorly understood, especially when TRPC3 also regulates TGF-ß. To address this issue, researchers have identified SIRT1 as a modulator of the transcription of TGF-ß-dependent genes, which participate in the process of fibrosis [22] .…”
Section: Sirt1 Is An Trpc3-interacting Partnermentioning
confidence: 99%
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“…Calcium overload and reactive oxygen species (ROS) generation were two main mechanisms of myocardial stunning [87]. ROS has significant relationship with myocardial fibrosis [89]. Nowadays, myocardial native T1 times on cardiac MRI have been shown to be a surrogate marker of myocardial fibrosis [90].…”
Section: Electrolyte Disorder and Hemodialysismentioning
confidence: 99%
“…9 Canonical transient receptor potential receptor 3 (TRPC3) is an indispensable factor in regulating the mechanisms of fibrosis development and in promoting the transition of fibroblasts into myofibroblasts with an adverse influence on the modulation of collagen. 10 Interestingly, TRPC3 is directly activated by PKC phosphorylation. We speculated that Hcy could trigger TRPC3 to mediate the mechanism of atrial fibrosis.…”
mentioning
confidence: 99%