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Retracted : HO‐1 overexpression alleviates senescence by inducing autophagy via the mitochondrial route in human nucleus pulposus cells
Author(s) -
Yi Weiwei,
Lan Haiyang,
Wen Yafeng,
Wang Yiyang,
He Danshuang,
Bai Zhibiao,
Zhang Ye,
Jiang Wei,
Liu Bo,
Shen Jieliang,
Hu Zhenming
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29684
Subject(s) - autophagy , microbiology and biotechnology , senescence , mitochondrion , apoptosis , programmed cell death , cell , chemistry , biology , biochemistry
Intervertebral disc degeneration (IDD) is closely associated with aging. Our previous studies have confirmed that heme oxygenase‐1 (HO‐1) can inhibit nucleus pulposus (NP) cell apoptosis. However, whether or not HO‐1 is involved in NP cell senescence and autophagy is unclear. Our results indicated that HO‐1 expression was reduced in IDD tissues and replicative senescent NP cells. HO‐1 overexpression using a lentiviral vector reduced the NP cell senescence level, protected mitochondrial function, and promoted NP cell autophagy through the mitochondrial pathway. Autophagy inhibitor 3‐MA pretreatment reversed the anti‐senescent and protective effects on the mitochondrial function of HO‐1, which promoted the degradation of the extracellular matrix (ECM) in the intervertebral disc. In vivo, HO‐1 overexpression inhibited IDD and enhanced autophagy. In summary, these results suggested that HO‐1 overexpression alleviates NP cell senescence by inducing autophagy via the mitochondrial route.