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Review
. 2019 Sep 9;11(17):7307-7327.
doi: 10.18632/aging.102247. Epub 2019 Sep 9.

Metabolic remodeling induced by mitokines in heart failure

Jiahao Duan  1 , Zijun Chen  1 , Yeshun Wu  1 , Bin Zhu  2 , Ling Yang  1 , Chun Yang  3
Affiliations
Review

Metabolic remodeling induced by mitokines in heart failure

Jiahao Duan et al. Aging (Albany NY). .

Abstract

The prevalence rates of heart failure (HF) are greater than 10% in individuals aged >75 years, indicating an intrinsic link between aging and HF. It has been recognized that mitochondrial dysfunction contributes to the pathology of HF. Mitokines are a type of cytokines, peptides, or signaling pathways produced or activated by the nucleus or the mitochondria through cell non-autonomous responses during cellular stress. In addition to promoting the communication between the mitochondria and the nucleus, mitokines also exert a systemic regulatory effect by circulating to distant tissues. It is noteworthy that increasing evidence has demonstrated that mitokines are capable of reducing the metabolic-related HF risk factors and are associated with HF severity. Consequently, mitokines might represent a potential therapy target for HF.

Keywords: heart; metabolism; mitohormesis; peptides; retrograde signaling.

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Conflict of interest statement

CONFLICTS OF INTEREST: The authors declare that they have no conflicts of interests.

Figures

Figure 1
Figure 1
Small molecules arising from the mitochondria served as cellular and systemic signals. ATP: adenosine triphosphate; ADP: adenosine diphosphate; AMP: adenosine monophosphate; AMPK: 5' adenosine monophosphate-activated protein kinase; CaU: calcium uniporter; e-: electron; HIF-1α: hypoxia-inducible factor 1-alpha; IL-1β: interleukin 1 beta; mtDNA: mitochondrial deoxyribonucleic acid; MOMP: mitochondrial outer membrane permeabilization; MPTP: mitochondrial permeability transition pore; NLRP3: nucleotide-binding oligomerization domain-like receptors pyrin domain containing 3; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells; NADH: nicotinamide adenine dinucleotide; OS: oxidative stress; Q: ubiquinone; QH2: ubiquinol; ROS: reactive oxygen species; SIRT1: sirtuin1; SIRT3: sirtuin3; SIRT6: sirtuin6; SDH: succinate dehydrogenase.
Figure 2
Figure 2
Communication between mitochondria and nucleus in heart failure. ATP: adenosine triphosphate; ADP: adenosine diphosphate; ATF5: activating transcription factor 5; DNA: deoxyribonucleic acid; ETC: electron transfer chain; FAO: fatty acid β-oxidation; FADH2: reduced flavin adenine dinucleotide; FGF21: fibroblast growth factor 21; GDF15: growth differentiation factor 15; Mt: mitochondrial; MDPs: mitochondria-derived peptides; NADH: nicotinamide adenine dinucleotide; OS: oxidative stress; OXPHOS: oxidative phosphorylation; ROS: reactive oxygen species; UPRmt: mitochondrial unfolded protein response.
Figure 3
Figure 3
Systematic metabolism regulated by cell non-autonomous effect. FGF21: fibroblast growth factor 21; GDF15: growth differentiation factor 15; GI: gastrointestinal; MDPs: mitochondria-derived peptides; UPRmt: mitochondrial unfolded protein response.
See this image and copyright information in PMC

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