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Mitochondrial Mechanosensor Microdomains in Cardiovascular Disorders

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Mitochondrial Dynamics in Cardiovascular Medicine

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 982))

Abstract

The cardiomyocytes populating the ‘working myocardium’ are highly organized and such organization ranges from macroscale (e.g. the geometrical rod shape) to microscale (dyad/t-tubules) domains. This meticulous level of organization is imperative for assuring the normal and physiological pump-function of the heart. In the pathological cardiac tissue, the domains-related architecture is partially lost, resulting in morphological, electrical and metabolic remodeling and promoting cardiovascular diseases including heart failure and arrhythmias. Indeed, arrhythmogenesis during heart failure is a major clinical problem. Arrhythmias have been extensively studied from an electrical etiology, but only recently, physiologists and scientists have focused their attention on cellular and subcellular mechanosensors. We and others have investigated whether the nanoscale mechanosensitive properties of cardiomyocytes from failing hearts have a bearing upon the initiation of abnormal electrical activity. This chapter highlights the recent findings in the field, especially the role of mitochondria function and alignment in failing cardiomyocytes interrogated via nanomechanical stimuli.

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Authors and Affiliations

  1. Department of Medicine and Surgery, University of Parma, Parma, 43124, Italy

    Michele Miragoli & Aderville Cabassi

  2. Humanitas Clinical and Research Center, Rozzano, MI, Italy

    Michele Miragoli

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  1. Michele Miragoli
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  2. Aderville Cabassi
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Correspondence to Michele Miragoli .

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  1. Dept. of Biomedical Advanced Sciences, Federico II University, Naples, Italy

    Gaetano Santulli

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Miragoli, M., Cabassi, A. (2017). Mitochondrial Mechanosensor Microdomains in Cardiovascular Disorders. In: Santulli, G. (eds) Mitochondrial Dynamics in Cardiovascular Medicine. Advances in Experimental Medicine and Biology, vol 982. Springer, Cham. https://doi.org/10.1007/978-3-319-55330-6_13

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