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Figure 3. Proteins that induce UPR^mt activation in young and aged damaged cardiomyocytes and their role in mitochondrial function. Proteins that promote UPR^mt activation in young, damaged cardiomyocytes are illustrated in blue, and aged cardiomyocytes in yellow. Proteins common to both age groups, which activate UPR^mt, are represented in green. In young, damaged myocytes, mitochondrial respiration and biogenesis are decreased, while mitophagy is increased (pink squares). In contrast, in aged cardiac cells, mitochondrial bioenergetics improve and mitophagy decreases following UPR^mt activation by the Lon1 peptidase (LonP1), yeast mitochondrial escape 1-like-1 (YME1L), and fibroblast growth factor 21/sirtuin-3 (FGF21/SIRT3, purple squares). HSP: Heat shock protein; ATF5: transcription factor-5; FUNDC1: FUN14 domain containing 1; DIO2: type II deiodinase; ClpP: mitochondrial caseinolytic protease P; Oma1: stress-activated protease 1 m-AAA; CHOP: C/EBP homologous protein; HtrA2: high-temperature requirement protein A2; DDIT3: DNA damage-inducible transcript 3; UBL5: ubiquitin-like protein 5; OPA1: optic atrophy protein 1; Fis1: mitochondrial fission protein 1. Created using BioRender (www.app.biorender.com).