SPI1 activates mitochondrial unfolded response signaling to inhibit chondrocyte senescence and relieves osteoarthritis.

Xiangyu Zu, Shenghong Chen, Zhengyuan Li, Lin Hao, Wenhan Fu, Hui Zhang, Zongsheng Yin, Yin Wang, Jun Wang

Department of Oncology, The First Affiliated Hospital of Anhui Medical University, Anhui, China.Department of Oncology, The First Affiliated Hospital of Anhui Medical University, Anhui, China. · pubmed

Paper

Abstract

Chondrocyte senescence is a critical pathological hallmark of osteoarthritis (OA). Aberrant mechanical stress is considered a pivotal determinant in chondrocyte aging; however, the precise underlying mechanism remains elusive. Our findings demonstrate that SPI1 plays a significant role in counteracting chondrocyte senescence and inhibiting OA progression. SPI1 binds to the PERK promoter, thereby promoting its transcriptional activity. Importantly, PERK, rather than GCN2, facilitates eIF2α phosphorylation, activating the mitochondrial unfolded protein response (UPR

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Research summary

SPI1 activation of mitochondrial unfolded response signaling inhibits chondrocyte senescence and alleviates osteoarthritis. The paper addresses a mechanism that could potentially mitigate a key aspect of aging-related degeneration in cartilage, linking it to longevity research.

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