ReviewNaunyn-Schmiedeberg's archives of pharmacology2008
Roles of TRP channels in the development of cardiac hypertrophy.
Review in Naunyn-Schmiedeberg's archives of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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.
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.
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Who cites it
30 citing papers in PubMed, 60 citations in OpenAlex.
- Pathophysiological significance and modulation of the transient receptor potential canonical 3 ion channel.Medicinal research reviews · 2024Review
- Targeting mitochondrial shape: at the heart of cardioprotection.Basic research in cardiology · 2023Article
- Transient Receptor Potential Canonical 6 (TRPC6) Channel in the Pathogenesis of Diseases: A Jack of Many Trades.Inflammation · 2023Review
- Drug repurposing for the treatment of COVID-19.Journal of pharmacological sciences · 2022Review
- TRPC1 channels underlie stretch-modulated sarcoplasmic reticulum calcium leak in cardiomyocytes.Frontiers in physiology · 2022Article
- Remedia Sternutatoria over the Centuries: TRP Mediation.Molecules (Basel, Switzerland) · 2021Review
- Does Transient Receptor Potential Vanilloid Type 1 Alleviate or Aggravate Pathological Myocardial Hypertrophy?Frontiers in pharmacology · 2021Review
- Canonical Transient Receptor Potential Channels and Vascular Smooth Muscle Cell Plasticity.Journal of lipid and atherosclerosis · 2020Review
- TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling.Frontiers in physiology · 2019Review
- Review
- The Pattern of mRNA Expression Is Changed in Sinoatrial Node from Goto-Kakizaki Type 2 Diabetic Rat Heart.Journal of diabetes research · 2018Article
- TRPC6 counteracts TRPC3-Nox2 protein complex leading to attenuation of hyperglycemia-induced heart failure in mice.Scientific reports · 2017Article
- TRPC3-Nox2 complex mediates doxorubicin-induced myocardial atrophy.JCI insight · 2017Article
- Deletion of TRPC6 Attenuates NMDA Receptor-Mediated CaFrontiers in neuroscience · 2017Article
- TRPC3 Channels in Cardiac Fibrosis.Frontiers in cardiovascular medicine · 2017Review
- TRPC3 positively regulates reactive oxygen species driving maladaptive cardiac remodeling.Scientific reports · 2016Article
- "TRP inflammation" relationship in cardiovascular system.Seminars in immunopathology · 2016Review
- Different Profile of mRNA Expression in Sinoatrial Node from Streptozotocin-Induced Diabetic Rat.PloS one · 2016Article
- Article
- Transient receptor potential (TRP) channels and cardiac fibrosis.Current topics in medicinal chemistry · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy is induced by various stresses such as hypertension and myocardial infarction. It is believed that hypertrophy is adaptive in the early phase but becomes maladaptive in the late phase. Cardiac hypertrophy develops heart failure when the heart is exposed persistently to the stresses. The increase in intracellular Ca(2+) ([Ca(2+)](i)) plays an important role in the development of hypertrophy. It is generally thought that the increase in [Ca(2+)](i) for hypertrophy occurs via G(q)-stimulated production of inositol-1,4,5-trisphosphate (IP(3)) and IP(3)-mediated release of Ca(2+) from intracellular store. However, several groups recently reported that canonical transient receptor potential (TRPC) channels are responsible for the increase in [Ca(2+)](i). Among them, three TRPC subtypes (TRPC3/TRPC6/TRPC7) are activated by another G(q)-mediated second messenger, diacylglycerol. Although several groups independently demonstrated that TRPC channels mediate receptor-stimulated and pressure overload-induced hypertrophy, there is discrepancy of which subtypes of TRPC channels predominantly mediate hypertrophy. However, there is consensus that TRPC-mediated Ca(2+) influx is essential for hypertrophy. As TRPC channels participate in pathological hypertrophy, but not physiological contraction and the relaxation cycle, TPRC channels are a new target for the treatment of hypertrophy.
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Registered trials
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.