olivier cazorla PhD physiology

Course and current status

Research Director, Centre National de la Recherche Scientifique (CNRS)- 2018.

Chargé de Recherche (senior governmental research position) in Centre National de la Recherche Scientifique (CNRS)- 2002-217.

Research-associate in Dr. Guy Vassort laboratory, INSERM U390, Montpellier, FRANCE . 2001-2002 « Titin and heart failure: alteration of Frank-Starling relationship». 

Research-associate in Dr. Henk Granzier laboratory, Washington State University, Pullman USA. 1998-2001 « Physiological role of titin isoform co-expression in the heart».


PhD, university of Tours, 1998- supervisors Prof D. Garnier & JY Le Guennec."Length-tension relationship of mammalian isolated cardiomyocyte: importance of regionalisation and role of titin".

Habilitation à Diriger les Recherches (HDR), 2007, University of Montpellier I, France.


Current lab: "Physiologie et Médecine Expérimentale du cœur et des Muscles"

Inserm U1046-UMR CNRS 9214-Université de Montpellier, CHU Arnaud de Villeneuve Montpellier, France

Team Arnaud Bourdin : Respiratory diseases and environment -

Expertise & distinction:

Editorial board “ Pflugers Arch., European Journal of Physiology ”  (2011-2014; 2016-) and Journal of Muscle Research and Cell Motility (2016-), “Journal of Molecular and cellular cardiology” (2019-)

PhD Fellow from the french Ministery of research and technology (1995-1998), Post-doctoral Fellow of AHA (1998-2001), Fellow of Fondation Philippe (2000), Fellow of FRM (2001-2002)

Elected Member of the national committee of CNRS, section 24 (2012-2016)

Bronze Medal of CNRS (2011)

Prime d’Excellence Scientifique (2012-2016)

Scientific summary

Cardiac contraction is determined by the amount of calcium (Ca2+) released by the reticulum sarcoplasmic and by the Ca2+ sensitivity of the contractile machinery that increases proportionally to the end-diastolic ventricular volume. This latter phenomenon, known as the Frank-Starling relationship, originates from cell adaptation to acute stretch involving a sarcomere length (SL) dependence of the Ca2+ sensitivity of myofilament activation. However, the molecular basis of this mechanism is still unclear. Furthermore, this regulation is altered during various cardiac pathologies consecutive to either heart diseases (ischemia, pressure overload…) or genetic muscular diseases (cardiomyopathies) and contributes to cardiac insufficiency. It is thus important to determine the signaling pathways activated by acute stretch of the myocardium and the steps altered during those pathologies in order to prevent or to correct them. Works from several groups including early results from our laboratory reported that various kinases and phosphatases modulate contractile activity at the myofilament level. More recently, we have shown that: 1/ Myosin light chain 2 (MLC2 a regulatory protein of the myofilaments) phosphorylation increases during sarcomere lengthening. 2/ This regulation is mainly present in the sub-endocardial layer in the free wall of the left ventricle according to a positive linear gradient from sub-epi to sub-endocardial layers. 3/ This gradient disappears in pathological conditions (post-myocardial infarction, PMI).

We are now interested to determine the direct and indirect impacts of air pollution on the coupling of lung function and cardiovascular hemodynamics in humans and in animal models. Indeed air pollution is a public health problem with respiratory and cardiovascular consequences. We have previously shown that chronic exposure to levels of carbon monoxide relevant to the city environment worsens ischemic heart failure and negatively affects cardiac function, even in the absence of sub-heart disease. underlying. These results demonstrate a direct link between air pollution and pulmonary / cardiovascular disease that we aim to study.

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