Evidence map›Paper›PMID 30848206›Full record

ReviewCurrent cardiology reviews2019

Physiological and Pathological Role of TRPV1, TRPV2 and TRPV4 Channels in Heart.

Alexandr S Gorbunov, Leonid N Maslov, Amteshwar S Jaggi, Nirmal Singh, Luciano De Petrocellis, Alla A Boshchenko, Ali Roohbakhsh, Vladimir V Bezuglov, Peter R Oeltgen

Open access · greenAbstract readReview
In one paragraph

Review in Current cardiology reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 28% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  4. Tapered fiber probe-based optical cardiac pacemaker.Frontiers in bioengineering and biotechnology · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 6 institutions in 5 countries.

Alexandr S GorbunovLaboratory of Experimental Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center of The Russian Academy of Science, Tomsk, Russian Federation.
Leonid N MaslovLaboratory of Experimental Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center of The Russian Academy of Science, Tomsk, Russian Federation.
Amteshwar S JaggiDepartment of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, India.
Nirmal SinghDepartment of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, India.
Luciano De PetrocellisIstituto di Chimica Biomolecolare, Consiglio Nazionale delle Ricerche, Pozzuoli (NA), Italy.
Alla A BoshchenkoLaboratory of Experimental Cardiology, Cardiology Research Institute, Tomsk National Research Medical Center of The Russian Academy of Science, Tomsk, Russian Federation.
Ali RoohbakhshPharmaceutical Research Center, Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran.
Vladimir V BezuglovInstitute of Bioorganic Chemistry, acad. M.M. Shemyakin and Yu.A. Ovchinnikova RAS, Moscow, Russian Federation.
Peter R OeltgenDepartment of Pathology, University of Kentucky College of Medicine, Lexington, KY, United States.
Tomsk National Research Medical Center · RUPunjabi University · INInstitute of Bioorganic Chemistry · RUIstituto di Chimica Biomolecolare · ITMashhad University of Medical Sciences · IRUniversity of Kentucky · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transient receptor potential vanilloid channel 2 (TRPV2) is required for normal cardiac contractility. The stimulation of TRPV1 in isolated cardiomyocytes can aggravate the effect of hypoxia/ reoxygenation (H/R) on H9C2 cells. The knockout of the TRPV1 gene promotes increased tolerance of the isolated perfused heart to the impact of ischemia/reperfusion (I/R). However, activation of TRPV1 increases the resistance of the heart to I/R due to calcitonin gene-related peptide (CGRP) release from afferent nerve endings. It has been established that TRPV1 and TRPV2 are involved in the pathogenesis of myocardial infarction and, in all likelihood, ensure the cardiac tolerance to the ischemia/reperfusion. It has also been documented that the activation of TRPV4 negatively affects the stability of cardiomyocytes to the H/R. The blockade of TRPV4 can be considered as a new approach to the prevention of I/R injury of the heart. Studies also indicate that TRPV1 is involved in the pathogenesis of cardiac hypertrophy and that TRPV2 channels participate in the pathogenesis of dilated cardiomyopathy. Excessive expression of TRPV2 leads to chronic Ca2+- overload of cardiomyocytes, which may contribute to the development of cardiomyopathy.

Indexed as

HeartHumansTRPV Cation ChannelsTRPV1 protein, humanTRPV2 protein, humanTRPV4 protein, humanTRPV Cation Channelscardiomyocytescardiomyopathy.HeartTRPV1TRPV2TRPV4

Identifiers

PMID30848206
PMCPMC8142357
OpenAlexW2921717581

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.