ReviewJournal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology
Integration of pathways that signal cardiac growth with modulation of myofilament activity.
Review in Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 19 citations in OpenAlex.
- The p21-activated kinase 1 (Pak1) signalling pathway in cardiac disease: from mechanistic study to therapeutic exploration.British journal of pharmacology · 2018Review
- Influence of a constitutive increase in myofilament Ca(2+)-sensitivity on Ca(2+)-fluxes and contraction of mouse heart ventricular myocytes.Archives of biochemistry and biophysics · 2014Article
- Myofilament length dependent activation.Journal of molecular and cellular cardiology · 2010Review
- Phosphorylation of contractile proteins in response to alpha- and beta-adrenergic stimulation in neonatal cardiomyocytes.Translational research : the journal of laboratory and clinical medicine · 2010Article
- The role of Akt/GSK-3beta signaling in familial hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology · 2009Article
- Protein kinase C zeta. A novel regulator of both phosphorylation and de-phosphorylation of cardiac sarcomeric proteins.The Journal of biological chemistry · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We review evidence for integrated effects of the signals that promote cardiac growth and remodeling and that modify the processes of excitation-contraction coupling. We have focused on integration of alterations in myofilament function with cell growth on the basis of genetic linkage analysis demonstrating that sarcomeric mutations are causal in hypertrophic cardiomyopathies. This evidence argues strongly for a path of communication between the intrinsic functional changes associated with a sarcomeric protein mutation and nuclear events. Our hypothesis is that this communication is also essential to the transduction of extrinsic signals leading to hypertrophy and failure. Understanding this network of signaling pathways is certain to lead to better diagnostic and treatment approaches to heart failure.
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.