ReviewJournal of molecular and cellular cardiology2011
Three 4-letter words of hypertension-related cardiac hypertrophy: TRPC, mTOR, and HDAC.
Review in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Narrative review of metabolomics in cardiovascular disease.Journal of thoracic disease · 2021Review
- Sphingolipid Mediators of Myocardial Pathology.Journal of lipid and atherosclerosis · 2020Review
- The functional consequences of sodium channel NaESC heart failure · 2019Article
- Angiotensin II Signal Transduction: An Update on Mechanisms of Physiology and Pathophysiology.Physiological reviews · 2018Review
- Myocardial CKIP-1 Overexpression Protects from Simulated Microgravity-Induced Cardiac Remodeling.Frontiers in physiology · 2018Article
- Sodium Butyrate Protects -Against High Fat Diet-Induced Cardiac Dysfunction and Metabolic Disorders in Type II Diabetic Mice.Journal of cellular biochemistry · 2017Article
- Human GRK4γ142V Variant Promotes Angiotensin II Type I Receptor-Mediated Hypertension via Renal Histone Deacetylase Type 1 Inhibition.Hypertension (Dallas, Tex. : 1979) · 2016Article
- The CXCL10/CXCR3 Axis and Cardiac Inflammation: Implications for Immunotherapy to Treat Infectious and Noninfectious Diseases of the Heart.Journal of immunology research · 2016Review
- Quality control systems in cardiac aging.Ageing research reviews · 2015Review
- IGF-2R-Gαq signaling and cardiac hypertrophy in the low-birth-weight lamb.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
- Cardiac energy dependence on glucose increases metabolites related to glutathione and activates metabolic genes controlled by mechanistic target of rapamycin.Journal of the American Heart Association · 2015Article
- Deficiency of cardiac Acyl-CoA synthetase-1 induces diastolic dysfunction, but pathologic hypertrophy is reversed by rapamycin.Biochimica et biophysica acta · 2014Article
- LIF and the heart: just another brick in the wall?European cytokine network · 2013Review
- Perspectives of Targeting mTORC1-S6K1 in Cardiovascular Aging.Frontiers in physiology · 2012Article
- Adaptive mechanisms to compensate for overnutrition-induced cardiovascular abnormalities.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Left ventricular hypertrophy due to hypertension represents a major risk factor for adverse cardiovascular events and death. In recent years, the prevalence of cardiac hypertrophy has increased due to obesity and an aging population. Notably, a significant number of individuals have persistent cardiac hypertrophy in the face of blood pressure that is normalized by drug treatment. Thus, a better understanding of the processes underlying the cardiac remodeling events that are set into play by hypertension is needed. At the level of the cardiac myocytes, hypertrophic growth is often described as physiological, as occurs with exercise, or pathological, as seen with hypertension. Here we discuss recent developments in three areas that are fundamental to pathological hypertrophic growth of cardiac myocytes. These areas are the transient receptor potential canonical (TRPC) channels, mammalian target of rapamycin (mTOR) complexes, and histone deacetylase (HDAC) enzymes. In the last several years, studies in each of these areas have yielded new and exciting discoveries into the genesis of pathological growth of cardiac myocytes. The phosphoinositide 3-kinase-Akt signaling network may be the common denominator that links these areas together. Defining the interrelationship among TRPC channels, mTOR signaling, and HDAC enzymes is a promising, but challenging area of research. Such knowledge will undoubtedly lead to new drugs that better prevent or reverse left ventricular hypertension.
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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.