ArticleCellular logistics2012
Novel roles of PAK1 in the heart.
Article in Cellular logistics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 17 citations in OpenAlex.
- Cardiomyocyte Rac1 signaling in hypertrophy, arrhythmia, and cardiac stress adaptation.Journal of molecular and cellular cardiology plus · 2025Review
- PAK1 and Therapy Resistance in Melanoma.Cells · 2023Review
- Targeting p21-activated kinase 1 for development of a novel anti-arrhythmic drug class.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- MicroRNA-145 targets in cancer and the cardiovascular system: evidence for common signaling pathways.Vascular biology (Bristol, England) · 2020Review
- Murine Electrophysiological Models of Cardiac Arrhythmogenesis.Physiological reviews · 2017Review
- Gene regulation, alternative splicing, and posttranslational modification of troponin subunits in cardiac development and adaptation: a focused review.Frontiers in physiology · 2014Review
- Role of p21-activated kinases in cardiovascular development and function.Cellular and molecular life sciences : CMLS · 2013Review
- The PAKs come of age: Celebrating 18 years of discovery.Cellular logistics · 2012Article
- The differential effects of FTY720 on functional recovery and infarct size following myocardial ischaemia/reperfusion.Cardiovascular journal of AfricaArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
Abstract
Our work and others' over the past few years have led to the identification of new roles of PAK1 in cardiac physiology, such as the regulation of cardiac ion channel and actomyosin function. More recent studies have revealed that PAK1-deficient mice were vulnerable to cardiac hypertrophy and readily progress to failure under sustained pressure overload and susceptible to ischemia/reperfusion injury. Our further study indicated that the PAK1 activator FTY720 was able to prevent this pressure overload-induced hypertrophy in wild-type mice without compromising their cardiac functions. A cardiac protective effect against ischemia/reperfusion injury by FTY720 was also observed in both rat and mouse models by us and others. Thus, these studies suggest that PAK1 is more important in the heart than previously thought, in particular a therapeutic potential of PAK1 activators. In the future, in-depth investigations are required to further substantiate our hypotheses on mechanisms for PAK1 function in the heart and to explore a therapeutic potential of FTY720 and other PAK1 activators in heart disease conditions.
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.