ArticleBasic research in cardiology2010
Expression of active protein phosphatase 1 inhibitor-1 attenuates chronic beta-agonist-induced cardiac apoptosis.
Article in Basic research in cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Cardiotropic AAV gene therapy for heart failure: a phase 1 trial.Nature medicine · 2025Article
- Current Landscape of Heart Failure Gene Therapy.Journal of the American Heart Association · 2019Review
- 17β-Estradiol and/or estrogen receptor alpha signaling blocks protein phosphatase 1 mediated ISO induced cardiac hypertrophy.PloS one · 2018Article
- Protein Phosphatase Inhibitor-1 Gene Therapy in a Swine Model of Nonischemic Heart Failure.Journal of the American College of Cardiology · 2017Article
- Profiling analysis of long non-coding RNAs in early postnatal mouse hearts.Scientific reports · 2017Article
- Human G109E-inhibitor-1 impairs cardiac function and promotes arrhythmias.Journal of molecular and cellular cardiology · 2015Article
- CXCR4 attenuates cardiomyocytes mitochondrial dysfunction to resist ischaemia-reperfusion injury.Journal of cellular and molecular medicine · 2015Article
- Pre-treatment with α-tocopherol and Terminalia arjuna ameliorates, pro-inflammatory cytokines, cardiac and apoptotic markers in myocardial infracted rats.Redox report : communications in free radical research · 2015Article
- Counteracting Protein Kinase Activity in the Heart: The Multiple Roles of Protein Phosphatases.Frontiers in pharmacology · 2015Review
- Cardiac I-1c overexpression with reengineered AAV improves cardiac function in swine ischemic heart failure.Molecular therapy : the journal of the American Society of Gene Therapy · 2014Article
- Heart failure-specific changes in protein kinase signalling.Pflugers Archiv : European journal of physiology · 2014Review
- Protein phosphatase 1 inhibitor-1 deficiency reduces phosphorylation of renal NaCl cotransporter and causes arterial hypotension.Journal of the American Society of Nephrology : JASN · 2014Article
- Eugenia jambolana pretreatment prevents isoproterenol-induced myocardial damage in rats: evidence from biochemical, molecular, and histopathological studies.Journal of medicinal food · 2014Article
- Chronic activation of the low affinity site of β1-adrenoceptors stimulates haemodynamics but exacerbates pressure-overload cardiac remodelling.British journal of pharmacology · 2013Article
- AAV9.I-1c delivered via direct coronary infusion in a porcine model of heart failure improves contractility and mitigates adverse remodeling.Circulation. Heart failure · 2013Article
- Active inhibitor-1 maintains protein hyper-phosphorylation in aging hearts and halts remodeling in failing hearts.PloS one · 2013Article
- Constitutive phosphorylation of inhibitor-1 at Ser67 and Thr75 depresses calcium cycling in cardiomyocytes and leads to remodeling upon aging.Basic research in cardiology · 2012Article
- The relationship between the MMP system, adrenoceptors and phosphoprotein phosphatases.British journal of pharmacology · 2012Review
- Phosphatase-1-inhibitor-1: amplifier or attenuator of catecholaminergic stress?Basic research in cardiology · 2010Article
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10 authors at 5 institutions in 4 countries.
Funding
Abstract
Cardiac apoptosis has been considered an important contributing factor to heart failure. Several subcellular mechanisms, including increased protein phosphatase 1 activity, have been suggested to induce apoptosis. Protein phosphatase 1 is regulated by an endogenous inhibitor-1 (I-1) that is activated upon phosphorylation at threonine 35 via protein kinase A. Here, we tested whether cardiac-specific overexpression of a constitutively active (T35D, AA 1-65) inhibitor-1 (I-1c), could also affect cardiac apoptosis and heart failure progression induced by prolonged beta-adrenergic stimulation. We found that either acute or chronic expression of I-1c reduced isoproterenol (ISO)-induced apoptosis assessed by nuclear condensation, TUNEL staining and DNA fragmentation. The beneficial effects of I-1c were associated with increased expression of the anti-apoptotic protein Bcl-2, decreased expression of the pro-apoptotic protein Bax and reduced levels of active caspases as well as increased activation of ERK. These findings suggest that mitochondrial signaling and ERK activation may be involved in the I-1c cardioprotective effects against apoptosis induced by prolonged beta-adrenergic stimulation.
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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.