ArticleAmerican journal of physiology. Heart and circulatory physiology2015
Loss of Rad-GTPase produces a novel adaptive cardiac phenotype resistant to systolic decline with aging.
Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Pharmacological or genetic inhibition of LTCC promotes cardiomyocyte proliferation through inhibition of calcineurin activity.NPJ Regenerative medicine · 2025Article
- Sympathetic Nervous System Regulation of Cardiac Calcium Channels.Handbook of experimental pharmacology · 2023Article
- Adrenergic Regulation of Calcium Channels in the Heart.Annual review of physiology · 2022Review
- L-type channel inactivation balances the increased peak calcium current due to absence of Rad in cardiomyocytes.The Journal of general physiology · 2021Article
- Rad-GTPase contributes to heart rate via L-type calcium channel regulation.Journal of molecular and cellular cardiology · 2021Article
- Myocardial-restricted ablation of the GTPase RAD results in a pro-adaptive heart response in mice.The Journal of biological chemistry · 2019Article
- Rad GTPase deletion attenuates post-ischemic cardiac dysfunction and remodeling.JACC. Basic to translational science · 2018Article
- Rad GTPase is essential for the regulation of bone density and bone marrow adipose tissue in mice.Bone · 2017Article
- Rad-deletion Phenocopies Tonic Sympathetic Stimulation of the Heart.Journal of cardiovascular translational research · 2016Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Rad-GTPase is a regulator of L-type calcium current (LTCC), with increased calcium current observed in Rad knockout models. While mouse models that result in elevated LTCC have been associated with heart failure, our laboratory and others observe a hypercontractile phenotype with enhanced calcium homeostasis in Rad(-/-). It is currently unclear whether this observation represents an early time point in a decompensatory progression towards heart failure or whether Rad loss drives a novel phenotype with stable enhanced function. We test the hypothesis that Rad(-/-) drives a stable nonfailing hypercontractile phenotype in adult hearts, and we examine compensatory regulation of sarcoplasmic reticulum (SR) loading and protein changes. Heart function was measured in vivo with echocardiography. In vivo heart function was significantly improved in adult Rad(-/-) hearts compared with wild type. Heart wall dimensions were significantly increased, while heart size was decreased, and cardiac output was not changed. Cardiac function was maintained through 18 mo of age with no decompensation. SR releasable Ca(2+) was increased in isolated Rad(-/-) ventricular myocytes. Higher Ca(2+) load was accompanied by sarco/endoplasmic reticulum Ca(2+) ATPase 2a (SERCA2a) protein elevation as determined by immunoblotting and a rightward shift in the thapsigargan inhibitor-response curve. Rad(-/-) promotes morphological changes accompanied by a stable increase in contractility with aging and preserved cardiac output. The Rad(-/-) phenotype is marked by enhanced systolic and diastolic function with increased SR uptake, which is consistent with a model that does not progress into heart failure.
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Registered trials
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