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. 2022 Feb 28;12(5):2445–2464. doi: 10.7150/thno.70588

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There are some strategies for delaying senescence with respect to organelle interaction, including maintaining calcium homeostasis, maintaining protein homeostasis, enhancing MQC, and improving anti-lipotoxicity effects. We can decrease mitochondrial calcium intake by repressing the expression of IP3R, MCU or PACS-2, and increasing the expression of calreticulin. Moreover, we can inhibit the overactivated UPR by 4-PBA to delay cellular senescence. Promoting lysosome-mediated autophagy by rapamycin is also effective. Furthermore, we can increase mitochondrial fission or mitophagy via DRP1 or PRKN, respectively, to enhance MQC. Moreover, by overexpressing DGA1 (encodes DGAT homologue in yeast) and LRO1 (encodes phospholipid:diacylglycerol O-acyltransferase in yeast), we can increase the number of LDs to decrease mitochondrial ROS and mitochondrial fragmentation caused by high amounts of fatty acids.