ArticleThe American journal of pathology2012
Short-term akt activation in cardiac muscle cells improves contractile function in failing hearts.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Temporal Dynamics of Extracellular Matrix Remodeling in Anthracycline-Induced Cardiotoxicity.Cells · 2025Review
- Polarized macrophages modulate cardiac structure and contractility under hypoxia in novel immuno-heart on a chip.APL bioengineering · 2025Article
- Enhancement of mitochondrial calcium uptake is cardioprotective against maladaptive hypertrophy by retrograde signaling uptuning Akt.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- From dried bear bile to molecular investigation of differential effects of bile acids inBrain, behavior, & immunity - health · 2023Review
- Effects of T3 Administration onTransplant international : official journal of the European Society for Organ Transplantation · 2023Article
- Interleukin 4/13 signaling in cardiac regeneration and repair.American journal of physiology. Heart and circulatory physiology · 2022Review
- The female syndecan-4Frontiers in cell and developmental biology · 2022Article
- Investigation of cardiovascular protective effect of Shenmai injection by network pharmacology and pharmacological evaluation.BMC complementary medicine and therapies · 2020Article
- Inhibition of the ROS-EGFR Pathway Mediates the Protective Action of Nox1/4 Inhibitor GKT137831 against Hypertensive Cardiac Hypertrophy via Suppressing Cardiac Inflammation and Activation of Akt and ERK1/2.Mediators of inflammation · 2020Article
- Elevated dual specificity protein phosphatase 4 in cardiomyopathy caused by lamin A/C gene mutation is primarily ERK1/2-dependent and its depletion improves cardiac function and survival.Human molecular genetics · 2018Article
- Mechanisms of Chinese Medicine Xinmailong's protection against heart failure in pressure-overloaded mice and cultured cardiomyocytes.Scientific reports · 2017Article
- Timing of the negative effects of trastuzumab on cardiac mechanics after anthracycline chemotherapy.The international journal of cardiovascular imaging · 2017Observational
- Low-intensity pulsed ultrasound enhances angiogenesis and ameliorates contractile dysfunction of pressure-overloaded heart in mice.PloS one · 2017Article
- PI3K Phosphorylation Is Linked to Improved Electrical Excitability in an In Vitro Engineered Heart Tissue Disease Model System.Tissue engineering. Part A · 2015Article
- The antioxidant compound tert-butylhydroquinone activates Akt in myocardium, suppresses apoptosis and ameliorates pressure overload-induced cardiac dysfunction.Scientific reports · 2015Article
- Adrenomedullin promotes differentiation of oligodendrocyte precursor cells into myelin-basic-protein expressing oligodendrocytes under pathological conditions in vitro.Stem cell research · 2015Article
- Physiological activation of Akt by PHLPP1 deletion protects against pathological hypertrophy.Cardiovascular research · 2015Article
- Total Flavonoids from Clinopodium chinense (Benth.) O. Ktze Protect against Doxorubicin-Induced Cardiotoxicity In Vitro and In Vivo.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Nitrite therapy improves left ventricular function during heart failure via restoration of nitric oxide-mediated cytoprotective signaling.Circulation research · 2014Article
- Tongxinluo protects against pressure overload-induced heart failure in mice involving VEGF/Akt/eNOS pathway activation.PloS one · 2014Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
Abstract
Akt is a serine/threonine protein kinase that is activated by a variety of growth factors or cytokines in a phosphatidylinositol 3-kinase-dependent manner. By using a conditional transgenic system in which Akt signaling can be turned on or off in the adult heart, we previously showed that short-term Akt activation induces a physiological form of cardiac hypertrophy with enhanced coronary angiogenesis and maintained contractility. Here we tested the hypothesis that induction of physiological hypertrophy by short-term Akt activation might improve contractile function in failing hearts. When Akt signaling transiently was activated in murine hearts with impaired contractility, induced by pressure overload or doxorubicin treatment, contractile dysfunction was attenuated in both cases. Importantly, improvement of contractility was observed before the development of cardiac hypertrophy, indicating that Akt activation improves contractile function independently of its growth-promoting effects. To gain mechanistic insights into Akt-mediated positive inotropic effects, transcriptional profiles in the heart were determined in a pressure overload-induced heart failure model. Biological network analysis of differentially expressed transcripts revealed significant alterations in the expression of genes associated with cell death, and these alterations were reversed by short-term Akt activation. Thus, short-term Akt activation improves contractile function in failing hearts. This beneficial effect of Akt on contractility is hypertrophy-independent and may be mediated in part by inhibition of cell death associated with heart failure.
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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.