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. 2021 Dec 1;12(8):2016–2030. doi: 10.14336/AD.2021.0427

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Copyright: © 2021 Liu et al.

this is an open access article distributed under the terms of the creative commons attribution license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Figure 1. — The potential mechanisms of mitochondrial quality control (MQC) dyshomeostasis in sarcopenia. Impaired mitochondrial proteostasis, biogenesis, dynamics and autophagy have been regarded as the major molecular mechanisms in mitochondrial dysfunction, which could lead to the onset and progression of sarcopenia. (PIK3: phosphoinositide 3-kinase; Akt: protein kinase B; mTOR: mechanistic target of rapamycin; FoxO: Forkhead Box O; MAFbx: muscle atrophy F-box; MuRF-1: muscle RING finger protein 1; PGC-1α: peroxisome proliferative activated receptor-γ coactivator-1α; Nrf-1 and 2: nuclear respiratory factor-1 and -2; ERRα: estrogen-related receptor alpha; Tfam: mitochondrial transcription factor A; NEMPs: nuclear-encoded mitochondrial proteins; mtDNA: mitochondrial DNA; Opa1: optic atrophy 1; Mfn1 and 2: mitofusin 1 and 2; Fis1: ﬁssion protein 1; Drp1: dynamin-related protein 1; Mff: mitochondrial ﬁssion factor; NIX: BCL2 interacting protein 3 like; BNIP3: BCL2 interacting protein 3; FUNDC1: FUN14 domain containing 1; PINK1: PTEN induced putative kinase 1; p62: sequestosome 1; LC 3: microtubule-associated protein light chain 3).