ReviewJournal of cardiovascular translational research2010
Revisited and revised: is RhoA always a villain in cardiac pathophysiology?
Review in Journal of cardiovascular translational research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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.
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
37 citing papers in PubMed, 51 citations in OpenAlex.
- Roles of small GTPases in cardiac hypertrophy (Review).Molecular medicine reports · 2024Review
- Untangling the role of RhoA in the heart: protective effect and mechanism.Cell death & disease · 2024Review
- RhoA signaling increases mitophagy and protects cardiomyocytes against ischemia by stabilizing PINK1 protein and recruiting Parkin to mitochondria.Cell death and differentiation · 2022Article
- Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022Review
- Review
- Review
- RhoA: a dubious molecule in cardiac pathophysiology.Journal of biomedical science · 2021Review
- Donor-specific phenotypic variation in hiPSC cardiomyocyte-derived exosomes impacts endothelial cell function.American journal of physiology. Heart and circulatory physiology · 2021Article
- Article
- RhoGTPase in Vascular Disease.Cells · 2019Review
- Adrenergic Regulation of Drp1-Driven Mitochondrial Fission in Cardiac Physio-Pathology.Antioxidants (Basel, Switzerland) · 2018Review
- How cardiomyocytes sense pathophysiological stresses for cardiac remodeling.Cellular and molecular life sciences : CMLS · 2017Review
- Nutrient-sensing mTORC1: Integration of metabolic and autophagic signals.Journal of molecular and cellular cardiology · 2016Review
- Phosphodiesterase inhibitor KMUP-3 displays cardioprotection via protein kinase G and increases cardiac output via G-protein-coupled receptor agonist activity and Ca(2+) sensitization.The Kaohsiung journal of medical sciences · 2016Article
- Endurance training in early life results in long-term programming of heart mass in rats.Physiological reports · 2016Article
- Hypoxic induction of T-type Ca(2+) channels in rat cardiac myocytes: role of HIF-1α and RhoA/ROCK signalling.The Journal of physiology · 2015Article
- The sarcomeric M-region: a molecular command center for diverse cellular processes.BioMed research international · 2015Review
- Rho/Rho-associated coiled-coil forming kinase pathway as therapeutic targets for statins in atherosclerosis.Antioxidants & redox signaling · 2014Review
- Prevention of RhoA activation and cofilin-mediated actin polymerization mediates the antihypertrophic effect of adenosine receptor agonists in angiotensin II- and endothelin-1-treated cardiomyocytes.Molecular and cellular biochemistry · 2014Article
- PLCε, PKD1, and SSH1L transduce RhoA signaling to protect mitochondria from oxidative stress in the heart.Science signaling · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The neonatal rat ventricular myocyte model of hypertrophy has provided tremendous insight with regard to signaling pathways regulating cardiac growth and gene expression. Many mediators thus discovered have been successfully extrapolated to the in vivo setting, as assessed using genetically engineered mice and physiological interventions. Studies in neonatal rat ventricular myocytes demonstrated a role for the small G-protein RhoA and its downstream effector kinase, Rho-associated coiled-coil containing protein kinase (ROCK), in agonist-mediated hypertrophy. Transgenic expression of RhoA in the heart does not phenocopy this response, however, nor does genetic deletion of ROCK prevent hypertrophy. Pharmacologic inhibition of ROCK has effects most consistent with roles for RhoA signaling in the development of heart failure or responses to ischemic damage. Whether signals elicited downstream of RhoA promote cell death or survival and are deleterious or salutary is, however, context and cell-type dependent. The concepts discussed above are reviewed, and the hypothesis that RhoA might protect cardiomyocytes from ischemia and other insults is presented. Novel RhoA targets including phospholipid regulated and regulating enzymes (Akt, PI kinases, phospholipase C, protein kinases C and D) and serum response element-mediated transcriptional responses are considered as possible pathways through which RhoA could affect cardiomyocyte survival.
Indexed as
Identifiers
What OpenQuestion holds
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.