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Darwinian evolution and cardiovascular remodeling

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Abstract

Mechanotransduction, MT, is an ancient evolutionary legacy existing in every living species and involving complex rearrangements of multiple proteins in response to a mechanical stress. MT includes three different interrelated processes: mechanosensation, mechanotransmission, and mechanoresponse. Each process is specifically adapted to a given tissue and stress. Both cardiac and arterial remodeling involve MT. Physiological or pathological cardiac remodeling, CR, is firstly a beneficial mechanoresponse, MR, which allows the heart to recover to a normal economy, better adapted to the new working conditions. Nevertheless, exercise-induced cardiac remodeling is more a coming-back to normal conditions than a superimposed event. On the longer term, the MR creates fibrosis which accounts, in part, for the reduced cardiac output in the CR. In the hypertension-induced arterial remodeling, arterial MR allows the vessels to maintain a normal circumferential constraint before an augmented arterial pressure. In atherogenesis: (i) The presence of atheroma in several animal species and atherosclerosis in ancient civilizations suggests more basic predispositions. (ii) The atherosclerotic plaques preferably develop at predictable arterial sites of disturbed blood flow showing that MT is involved in the initial steps of atherogenesis.

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References

  1. Nesse RM, Bergstrom CT, Ellison PT, Flier JS, Gluckman P, Govindaraju DR, Niethammer D, Omenn GS, Perlman RL, Schwartz MD, Thomas MG, Stearns SC, Valle D (2010) Making evolutionary biology a basic science for medicine. Proc Natl Acad Sci USA 107:1800–1816

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  2. Swynghedauw B (2016) Ch. 10 evolutionary paradigms in cardiology: the case of chronic heart failure. In: Alvergne A, Jenkinson C, Faurie C (eds) Evolutionary thinking in medicine, advances in the evolutionary analysis of human behavior. Springer International Publishing, Cham, pp 137–153

    Chapter  Google Scholar 

  3. Hoffman BD, Grashoff C, Schwartz MA (2011) Dynamic molecular process mediate cellular mechanotransduction. Nature 475:316–323

    Article  CAS  PubMed  Google Scholar 

  4. Orr AW, Helmke BP, Blackman BR, Schwartz MA (2006) Mechanisms of mechanotransduction. Dev Cell 10:11–20

    Article  CAS  PubMed  Google Scholar 

  5. DuFort CC, Paszek MJ, Weaver VM (2011) Balancing forces: architectural control of mechanotransduction. Nat Rev Mol Cell Biol 12:308–319

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  6. Isermann P, Lammerling J (2013) Nuclear mechanics and mechanotransduction. Review in health and disease. Curr Biol 2:R1113–R1121

    Article  Google Scholar 

  7. Jacob F (1977) Evolution and tinkering. Science 196:1161–1166

    Article  CAS  PubMed  Google Scholar 

  8. Fujiwara K, Masura M, Osawa MY, Kano Y, Katoh K (2001) Is PECAM-1 a mechanoresponsive molecule? Cell Struct Funct 26:11–17

    Article  CAS  PubMed  Google Scholar 

  9. Doolittle RF (1993) The evolution of vertebrate blood coagulation: a case of yin and yang. Thromb Haemost 70:24–28

    CAS  PubMed  Google Scholar 

  10. Swynghedauw B (1999) Molecular mechanisms of myocardial remodeling. Physiol Rev 79:215–262

    CAS  PubMed  Google Scholar 

  11. Lyon RC, Zanella F, Omens JH, Sheikh F (2015) Mechanotransduction in cardiac hypertrophy and failure. Circ Res 116:1462–1476

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  12. Swynghedauw B (2006) Phenotypic plasticity of adult myocardium. Molecular mechanisms. J Exp Biol 209:2320–2327

    Article  CAS  PubMed  Google Scholar 

  13. Takahashi K, Kakimoto Y, Toda K, Naruse K (2013) Mechanobiology in cardiac physiology and diseases. J Cell Mol Med 17:225–232

    Article  PubMed  PubMed Central  Google Scholar 

  14. Lompré AM, Schwartz K, d’Albis A, Lacombe G, Thiem NV, Swynghedauw B (1979) Myosin isoenzyme redistribution in chronic heart overloading. Nature 282:105–107

    Article  PubMed  Google Scholar 

  15. Alpert NR, Mulieri LA (1982) Increased myothermal economy of isometric force generation in compensated cardiac hypertrophy induced by pulmonary artery constriction in the rabbit. Circ Res 5:491–500

    Article  Google Scholar 

  16. Weber KT, Sun Y, Bhattachyara SK, Ahokas RA, Gerling IC (2013) Myofibroblast-mediated mechanisms of pathological remodeling of the heart. Nat Rev Cardiol 10:15–26

    Article  CAS  PubMed  Google Scholar 

  17. Creemers EE, Pinto YM (2011) Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart. Cardiovasc Res 89:265–272

    Article  CAS  PubMed  Google Scholar 

  18. Ellison GM, Waring CD, Vicinanza C, Torella D (2012) Physiological cardiac remodelling in response to endurance exercise training: cellular and molecular mechanisms. Heart 98:5–10

    Article  CAS  PubMed  Google Scholar 

  19. Booth FW, Gordon SE, Carlson CJ, Hamilton MT (2000) Waging war on modern chronic diseases: primary prevention through exercise biology. J Appl Physiol 88:774–787

    CAS  PubMed  Google Scholar 

  20. Williams TM, Bengtson P, Steller DL, Croll DA, Davis RW (2015) The healthy heart: lessons from nature’s elite athletes. Physiology 30:349–357

    Article  CAS  PubMed  Google Scholar 

  21. Moreira-Gonçalves D, Henriques-Coelho T, Fonseca H, Ferreira R, Padrao AI, Santa C, Vieira S, Silva AF, Amado F, Leite-Moreira A, Duarte JA (2015) Intermittent cardiac overload results in cardiac hypertrophy and provides protection against left ventricular acute pressure overload insult. J Physiol 593:3885–3897

    Article  PubMed  PubMed Central  Google Scholar 

  22. Bernardo BC, Weeks KI, Pretorius L, McMullen JR (2010) Molecular distinction between physiological and pathological cardiac hypertrophy. Experimental findings and therapeutic strategies. Pharmacol Ther 128:191–227

    Article  CAS  PubMed  Google Scholar 

  23. Benito BA, Gay-Jordi G, Serrano-Mollar A, Guasch E, Shi Y, Tardif JC, Brugada J, Nattel S, Mont L (2011) Cardiac arrhythmogenic remodeling in a rat model of long-term intensive exercise training. Circulation 123:13–22

    Article  PubMed  Google Scholar 

  24. Davies PF, Civelek M, Fang Y, Fleming I (2013) The athero-susceptible endothelium: endothelial phenotypes in complex haemodynamic shear stress regions in vivo. Cardiovasc Res 99:315–327

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  25. Conway DE, Schwartz MA (2013) Flow-dependent cellular mechano-transduction in atherosclerosis. J Cell Sci 126:5101–5109

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  26. Humphrey JD, Schwartz MA, Tellides G, Milewicz DM (2015) Role of mechanotransduction in vascular biology. Focus on thoracic aortic aneurysms and dissections. Circ Res 116:1448–1461

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  27. Vastesaeger MM, Delcourt R (1962) The natural history of atherosclerosis. Circulation 26:841–855

    Article  CAS  PubMed  Google Scholar 

  28. Thompson RC, Allam AH, Lombardi GP, Wann LS, Sutherland ML, Sutherland JD, Soliman MA, Frohlich B, Mininberg DT, Monge JM, Vallodolid CM, Cox SL, Abd el-Maksoud G, Badr I, Miyamoto MI, el-Halim Nur el-Din A, Narula J, Finch CE, Thomas GS (2013) Atherosclerosis across 4000 years of human history: the Horus study of four ancient populations. Lancet 381:1211–1222

    Article  PubMed  Google Scholar 

  29. Kwak BR, Bäck M, Bochaton-Piallat ML, Caligiuri G, Daemen Mat JAP, Davies PF, Hoefer IE, Holvoet P, Jo H, Krams R, Lehoux S, Monaco C, Steffens S, Virmani R, Weber C, Wentzel JJ, Evans PC (2014) Biomechanical factors in atherosclerosis: mechanisms and clinical implications. Eur Heart J 35:3013–3020

    Article  PubMed  PubMed Central  Google Scholar 

  30. Abe J-I, Berk BC (2014) Novel mechanisms of endothelial mechano-transduction. Arterioscler Thromb Vasc Biol 34:2378–2386

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  31. Swynghedauw B (2009) Quand le gène est en conflit avec son environnement. Une introduction à la médecine évolutionniste. De Boeck, Paris/Bruxelles

    Google Scholar 

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Correspondence to Bernard Swynghedauw.

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Swynghedauw, B. Darwinian evolution and cardiovascular remodeling. Heart Fail Rev 21, 795–802 (2016). https://doi.org/10.1007/s10741-016-9574-3

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