Viewpoints on the Role of Transient Receptor Potential Melastatin Channels in Cardiovascular System and Disease: A Systematic Review

Mirbod, Seyedeh Mahnaz; Khanahmad, Hossein; Amerizadeh, Atefeh; Amirpour, Afshin; Zaker, Erfan

doi:10.1016/j.cpcardiol.2021.101012

Cited by 4 publications

(3 citation statements)

References 77 publications

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“…We dug deeper into the mechanism by which TRPM4 causes vascular endothelial injury. Numerous TRP family members affect mitochondrial activity and generate excessive ROS, which leads to heart diseases ( Hof et al, 2019 ; Mirbod et al, 2023 ). The SUR1-TRPM4/NOS2/ROS signaling pathway mediates the inflammatory response in ischemia-reperfusion damage ( Maqoud et al, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

miR-133a-3p/TRPM4 axis improves palmitic acid induced vascular endothelial injury

Xue,

Tong,

Zhang

et al. 2024

Front. Pharmacol.

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Background: Vascular endothelial injury is a contributing factor to the development of atherosclerosis and the resulting cardiovascular diseases. One particular factor involved in endothelial cell apoptosis and atherosclerosis is palmitic acid (PA), which is a long-chain saturated fatty acid. In addition, transient receptor potential melastatin 4 (TRPM4), a non-selective cation channel, plays a significant role in endothelial dysfunction caused by various factors related to cardiovascular diseases. Despite this, the specific role and mechanisms of TRPM4 in atherosclerosis have not been fully understood.Methods: The protein and mRNA expressions of TRPM4, apoptosis - and inflammation-related factors were measured after PA treatment. The effect of TRPM4 knockout on the protein and mRNA expression of apoptosis and inflammation-related factors was detected. The changes of intracellular Ca2+, mitochondrial membrane potential, and reactive oxygen species were detected by Fluo-4 AM, JC-1, and DCFH-DA probes, respectively. To confirm the binding of miR-133a-3p to TRPM4, a dual luciferase reporter gene assay was conducted. Finally, the effects of miR-133a-3p and TRPM4 on intracellular Ca2+, mitochondrial membrane potential, and reactive oxygen species were examined.Results: Following PA treatment, the expression of TRPM4 increases, leading to calcium overload in endothelial cells. This calcium influx causes the assemblage of Bcl-2, resulting in the opening of mitochondrial calcium channels and mitochondrial damage, ultimately triggering apoptosis. Throughout this process, the mRNA and protein levels of IL-1β, ICAM-1, and VCAM1 significantly increase. Database screenings and luciferase assays have shown that miR-133a-3p preferentially binds to the 3′UTR region of TRPM4 mRNA, suppressing TRPM4 expression. During PA-induced endothelial injury, miR-133a-3p is significantly decreased, but overexpression of miR-133a-3p can attenuate the progression of endothelial injury. On the other hand, overexpression of TRPM4 counteracts the aforementioned changes.Conclusion: TRPM4 participates in vascular endothelial injury caused by PA. Therefore, targeting TRPM4 or miR-133a-3p may offer a novel pharmacological approach to preventing endothelial injury.

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Section: Discussionmentioning

confidence: 99%

miR-133a-3p/TRPM4 axis improves palmitic acid induced vascular endothelial injury

Xue,

Tong,

Zhang

et al. 2024

Front. Pharmacol.

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“…In this work, 6 hub TFGs (TRPV4, TRPV2, TRPC1, TRPC6, TRPC3, and TRPM8) were identified to serve as risky factors in HNSCC. TRP channel families are widely expressed in various tissues, regulating the multiple physiological process, and accumulating evidence has pointed out that they contribute to the regulation of carcinogenesis [ 19 , 20 ]. TRPV4 and TRPV2 both belong to vanilloid receptor-related subfamily.…”

Section: Discussionmentioning

confidence: 99%

A TRP Family Based Signature for Prognosis Prediction in Head and Neck Squamous Cell Carcinoma

Pan

Wang

Zheng

et al. 2022

Journal of Oncology

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Purpose. Head and neck squamous cell carcinoma (HNSCC) is a classical type of head and neck cancers, with heterogeneous clinical outcome. This project is set out to create a robust risk signature based on TRP family genes (TFGs) for prognosis evaluation in HNSCC. Methods. Based on the HNSCC sample data from the TCGA website, we integrated expression profile of TFGs for 490 HNSCC cases. We explore the interactions among TFGs using STRING tool. The TFGs-based signature (TFBS) was created by Cox relative analyses. In addition, we conducted GSEA to identify the underlying signaling pathways of the specific TFGs in HNSCC. The immune landscape of HNSCC patients was analyzed by CIBERSORT and ssGSEA algorithms. Results. A total of 6 TFGs (TRPC1, TRPC3, TRPC6, TRPV2, TRPV4, and TRPM8) closely associated with prognosis of HNSCC cases were screened to create TFBS. TFBS predicted that the TFBS-high group presented dismal patient outcome. Cox regression revealed the favorable independent value of TFBS. ROC analysis showed the robust power of TFBS for prognosis forecasting. GSEA determined several crucial pathways related with HNSCC, which are the p53 pathway, TNF-alpha signaling via NFKB, and hypoxia. Moreover, immune-related analysis showed that patients in the TFBS-high group were more likely in immunosuppressive status. Conclusion. Our proposed TFBS could serve as a favorable indicator to forecast the survival outcome of HNSCC cases and offer prominent therapy guidance.

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“…The TRPM subfamily is expressed in various organs and cells of the peripheral, central and immune systems and is vital in various biological processes, such as cold and heat stimulation, ion homeostasis, autophagy, vascular tension, epigenetics, and immune inflammation (29,(44)(45)(46)). An increasing number of studies have shown that TRPM channel participates in fibrotic diseases (47,48). (49).…”

Section: Trp Channels Classification and Functionmentioning

confidence: 99%

Multimodal roles of transient receptor potential channel activation in inducing pathological tissue scarification

Zheng,

Huang,

Zhang

et al. 2023

Front. Immunol.

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Transient receptor potential (TRP) channels are a class of transmembrane proteins that can sense a variety of physical/chemical stimuli, participate in the pathological processes of various diseases and have attracted increasing attention from researchers. Recent studies have shown that some TRP channels are involved in the development of pathological scarification (PS) and directly participate in PS fibrosis and re-epithelialization or indirectly activate immune cells to release cytokines and neuropeptides, which is subdivided into immune inflammation, fibrosis, pruritus and mechanical forces increased. This review elaborates on the characteristics of TRP channels, the mechanism of PS and how TRP channels mediate the development of PS, summarizes the important role of TRP channels in the different pathogenesis of PS and proposes that therapeutic strategies targeting TRP will be important for the prevention and treatment of PS. TRP channels are expected to become new targets for PS, which will make further breakthroughs and provide potential pharmacological targets and directions for the in-depth study of PS.

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Viewpoints on the Role of Transient Receptor Potential Melastatin Channels in Cardiovascular System and Disease: A Systematic Review

Cited by 4 publications

References 77 publications

miR-133a-3p/TRPM4 axis improves palmitic acid induced vascular endothelial injury

miR-133a-3p/TRPM4 axis improves palmitic acid induced vascular endothelial injury

A TRP Family Based Signature for Prognosis Prediction in Head and Neck Squamous Cell Carcinoma

Multimodal roles of transient receptor potential channel activation in inducing pathological tissue scarification

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