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Review
. 2020 Mar 24;9(3):892.
doi: 10.3390/jcm9030892.

Mitophagy in Cardiovascular Diseases

Giampaolo Morciano  1   2 , Simone Patergnani  1   2 , Massimo Bonora  2 , Gaia Pedriali  1   2 , Anna Tarocco  2   3 , Esmaa Bouhamida  2 , Saverio Marchi  4 , Gina Ancora  5 , Gabriele Anania  6 , Mariusz R Wieckowski  7 , Carlotta Giorgi  2 , Paolo Pinton  1   2
Affiliations
Review

Mitophagy in Cardiovascular Diseases

Giampaolo Morciano et al. J Clin Med. .

Abstract

Cardiovascular diseases are one of the leading causes of death. Increasing evidence has shown that pharmacological or genetic targeting of mitochondria can ameliorate each stage of these pathologies, which are strongly associated with mitochondrial dysfunction. Removal of inefficient and dysfunctional mitochondria through the process of mitophagy has been reported to be essential for meeting the energetic requirements and maintaining the biochemical homeostasis of cells. This process is useful for counteracting the negative phenotypic changes that occur during cardiovascular diseases, and understanding the molecular players involved might be crucial for the development of potential therapies. Here, we summarize the current knowledge on mitophagy (and autophagy) mechanisms in the context of heart disease with an important focus on atherosclerosis, ischemic heart disease, cardiomyopathies, heart failure, hypertension, arrhythmia, congenital heart disease and peripheral vascular disease. We aim to provide a complete background on the mechanisms of action of this mitochondrial quality control process in cardiology and in cardiac surgery by also reviewing studies on the use of known compounds able to modulate mitophagy for cardioprotective purposes.

Keywords: autophagy; cardiovascular diseases; mitochondria; mitophagy.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Molecular routes of mitophagy. Schematic representation of mitochondrial fate during mitophagy (upper panel). Representation of rearrangements of effectors onto the OMM in response to stress stimuli (lower left panel) and participants in the recruitment of the phogophore around the OMM (lower right panel) during mitophagy. OMM, outer mitochondrial membrane; FUNDC1, FUN14 Domain Containing 1; BNIP3, BCL2/adenovirus E1B 19 kDa protein-interacting protein 3; NIX, NIP-3-Like Protein X; PINK1, PTEN-induced kinase 1; PARKIN, Parkin RBR E3 Ubiquitin Protein Ligase; NDP52, Nuclear Domain 10 Protein 52; OPTN, Optineurin; LC3, Microtubule Associated Protein 1 Light Chain 3.
Figure 2
Figure 2
Involvement of mitophagy in major CVDs. Schematic representation of tissue remodeling during atherosclerosis (AS) (upper panel), I/R (middle panel) and heart failure (HF; lower panel) with related alterations in mitophagy extent, cell death or tissue remodeling. CVDs, cardiovascular diseases; I/R, ischemia/reperfusion; MPT, mitochondrial permeability transition; HF, heart failure.
See this image and copyright information in PMC

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