Recent progress in understanding mechanical stretch induced myocardial remodeling

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  • Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University,Shanghai 200032, China

Received date: 2019-04-26

  Online published: 2019-06-24

Abstract

Myocardial remodeling is an independent risk factor for major cardiovascular events such as heart failure. An abnormal increase in mechanical stress caused by hemodynamic pathological changes can directly trigger myocardial remodeling, accompanied by increased expression of neurohumoral factors, resulting in a synergistic effect which could further aggravate myocardial remodeling. Myocardial remodeling can be divided into pressure overload myocardial remodeling and volume overload myocardial remodeling, according to the type of mechanical stress overload. There are significant differences in the two types of myocardial remodeling at the gross structural, cellular, and molecular levels of the heart. Although volume overload is prevalent in various heart diseases, previous studies have focused on pressure overload myocardial remodeling, with a lack of sufficient elucidation of volume overload myocardial remodeling. It has been discovered through research that calcium-handling proteins and Akt may be held responsible for the difference between the two types of overload myocardial remodeling. This paper, which combines the previous achievements with our latest research results, outlines the similarities and differences between the two types of mechanical stress myocardial remodeling, attempts to shed some new light on precision research and personalized diagnosis and treatment of cardiac hypertrophy.

Cite this article

WU Jian , ZOU Yunzeng . Recent progress in understanding mechanical stretch induced myocardial remodeling[J]. Journal of Shanghai University, 2019 , 25(3) : 375 -380 . DOI: 10.12066/j.issn.1007-2861.2139

References

[1] Wu J, You J, Wang S , et al. Insights into the activation and inhibition of angiotensin Ⅱ type 1 receptor in the mechanically loaded heart[J]. Circ J, 2014,78(6):1283-1289.
[2] Te Riet L, Van Esch J H, Roks A J, et al. Hypertension: renin-angiotensin-aldosterone system alterations[J]. Circ Res, 2015,116(6):960-975.
[3] Toischer K, Rokita A G, Unsold B , et al. Differential cardiac remodeling in preload versus after load[J]. Circulation, 2010,122(10):993-1003.
[4] Davis J, Davis L C, Correll R N , et al. A tension-based model distinguishes hypertrophic versus dilated cardiomyopathy[J]. Cell, 2016,165(5):1147-1159.
[5] Olsen N T, Dimaano V L, Fritz-Hansen T , et al. Hypertrophy signaling pathways in experimental chronic aortic regurgitation[J]. J Cardiovasc Transl Res, 2013,6(5):852-860.
[6] Bartelds B, Borgdorff M A, Smit-Van Oosten A, et al. Differential responses of the right ventricle to abnormal loading conditions in mice: pressure vs. volume load[J]. Eur J Heart Fail, 2011,13(12):1275-1282.
[7] Bonow R O, Carabello B A, Chatterjee K , et al. 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons[J]. Circulation, 2008,118(15):e523-e661.
[8] Ago T, Yang Y, Zhai P , et al. Nifedipine inhibits cardiac hypertrophy and left ventricular dysfunction in response to pressure overload[J]. J Cardiovasc Transl Res, 2010,3(4):304-313.
[9] Plante E, Lachance D, Beaudoin J , et al. Comparative study of vasodilators in an animal model of chronic volume overload caused by severe aortic regurgitation[J]. Circ Heart Fail, 2009,2(1):25-32.
[10] You J, Wu J, Zhang Q , et al. Differential cardiac hypertrophy and signaling pathways in pressure versus volume overload[J]. Am J Physiol Heart Circ Physiol, 2018,314(3):H552-H562.
[11] Bers D M . Cardiac excitation-contraction coupling[J]. Nature, 2002,415(6868):198-205.
[12] Zou Y, Liang Y, Gong H , et al. Ryanodine receptor type 2 is required for the development of pressure overload-induced cardiac hypertrophy[J]. Hypertension, 2011,58(6):1099-1110.
[13] Zhang T, Maier L S, Dalton N D , et al. The deltaC isoform of CaMKⅡ is activated in cardiac hypertrophy and induces dilated cardiomyopathy and heart failure[J]. Circ Res, 2003,92(8):912-919.
[14] Zhang T, Zhang Y, Cui M , et al. CaMKⅡ is a RIP3 substrate mediating ischemia- and oxidative stress-induced myocardial necroptosis[J]. Nat Med, 2016, DOI: 10.1038/nm.4017.
[15] Suetomi T, Willeford A, Brand C S , et al. Inflammation and NLRP3 inflammasome activation initiated in response to pressure overload by Ca$^{2+}$/calmodulin-dependent protein kinase Ⅱ delta signaling in cardiomyocytes are essential for adverse cardiac remodeling[J]. Circulation, 2018,138(22):2530-2544.
[16] Sussman M A, Volkers M, Fischer K , et al. Myocardial AKT: the omnipresent nexus[J]. Physiol Rev, 2011,91(3):1023-1070.
[17] Moc C, Taylor A E, Chesini G P , et al. Physiological activation of Akt by PHLPP1 deletion protects against pathological hypertrophy[J]. Cardiovasc Res, 2015,105(2):160-170.
[18] Beltowski J . Leptin and the regulation of endothelial function in physiological and pathological conditions[J]. Clin Exp Pharmacol Physiol, 2012,39(2):168-178.
[19] Bernardo B C, Weeks K L, Pretorius L , et al. Molecular distinction between physiological and pathological cardiac hypertrophy: experimental findings and therapeutic strategies[J]. Pharmacol Ther, 2010,128(1):191-227.
[20] Wende A R, O'Neill B T, Bugger H, et al. Enhanced cardiac Akt/protein kinase B signaling contributes to pathological cardiac hypertrophy in part by impairing mitochondrial function via transcriptional repression of mitochondrion-targeted nuclear genes[J]. Mol Cell Biol, 2015,35(5):831-846.
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