Angiogenesis and cardiac hypertrophy: maintenance of cardiac function and causative roles in heart failure
- PMID: 24481846
- DOI: 10.1161/CIRCRESAHA.114.300507
Angiogenesis and cardiac hypertrophy: maintenance of cardiac function and causative roles in heart failure
Abstract
Cardiac hypertrophy is an adaptive response to physiological and pathological overload. In response to the overload, individual cardiac myocytes become mechanically stretched and activate intracellular hypertrophic signaling pathways to re-use embryonic transcription factors and to increase the synthesis of various proteins, such as structural and contractile proteins. These hypertrophic responses increase oxygen demand and promote myocardial angiogenesis to dissolve the hypoxic situation and to maintain cardiac contractile function; thus, these responses suggest crosstalk between cardiac myocytes and microvasculature. However, sustained pathological overload induces maladaptation and cardiac remodeling, resulting in heart failure. In recent years, specific understanding has increased with regard to the molecular processes and cell-cell interactions that coordinate myocardial growth and angiogenesis. In this review, we summarize recent advances in understanding the regulatory mechanisms of coordinated myocardial growth and angiogenesis in the pathophysiology of cardiac hypertrophy and heart failure.
Keywords: angiogenesis factor; anoxia; heart failure; hypertrophy; ischemia.
Similar articles
-
The role of Fas in the progression of ischemic heart failure: prohypertrophy or proapoptosis.Coron Artery Dis. 2008 Nov;19(7):527-34. doi: 10.1097/MCA.0b013e3283093707. Coron Artery Dis. 2008. PMID: 18923250 Review.
-
Lack of JunD promotes pressure overload-induced apoptosis, hypertrophic growth, and angiogenesis in the heart.Circulation. 2005 Sep 6;112(10):1470-7. doi: 10.1161/CIRCULATIONAHA.104.518472. Epub 2005 Aug 29. Circulation. 2005. PMID: 16129800
-
Syndecan-4 deficiency accelerates the transition from compensated hypertrophy to heart failure following pressure overload.Cardiovasc Pathol. 2017 May-Jun;28:74-79. doi: 10.1016/j.carpath.2017.03.008. Epub 2017 Mar 30. Cardiovasc Pathol. 2017. PMID: 28395201
-
Dissociation of hypertrophic growth from changes in myocyte contractile function.J Card Fail. 2002 Dec;8(6 Suppl):S415-20. doi: 10.1054/jcaf.2002.129252. J Card Fail. 2002. PMID: 12555154
-
Differences between pathological and physiological cardiac hypertrophy: novel therapeutic strategies to treat heart failure.Clin Exp Pharmacol Physiol. 2007 Apr;34(4):255-62. doi: 10.1111/j.1440-1681.2007.04585.x. Clin Exp Pharmacol Physiol. 2007. PMID: 17324134 Review.
Cited by
-
Sunitinib-induced cardiac hypertrophy and the endothelin axis.Theranostics. 2021 Feb 6;11(8):3830-3838. doi: 10.7150/thno.49837. eCollection 2021. Theranostics. 2021. PMID: 33664864 Free PMC article.
-
Endothelial derived, secreted long non-coding RNAs Gadlor1 and Gadlor2 aggravate cardiac remodeling.Mol Ther Nucleic Acids. 2024 Aug 15;35(3):102306. doi: 10.1016/j.omtn.2024.102306. eCollection 2024 Sep 10. Mol Ther Nucleic Acids. 2024. PMID: 39281699 Free PMC article.
-
Endothelial p53 deletion improves angiogenesis and prevents cardiac fibrosis and heart failure induced by pressure overload in mice.J Am Heart Assoc. 2015 Feb 24;4(2):e001770. doi: 10.1161/JAHA.115.001770. J Am Heart Assoc. 2015. PMID: 25713289 Free PMC article.
-
CYP2J2 and its metabolites (epoxyeicosatrienoic acids) attenuate cardiac hypertrophy by activating AMPKα2 and enhancing nuclear translocation of Akt1.Aging Cell. 2016 Oct;15(5):940-52. doi: 10.1111/acel.12507. Epub 2016 Jul 14. Aging Cell. 2016. PMID: 27416746 Free PMC article.
-
Inhibition of hypertrophy is a good therapeutic strategy in ventricular pressure overload.Circulation. 2015 Apr 21;131(16):1435-47. doi: 10.1161/CIRCULATIONAHA.115.013894. Circulation. 2015. PMID: 25901069 Free PMC article. Review. No abstract available.
Publication types
MeSH terms
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
