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<i>Retracted</i>: HO‐1 overexpression alleviates senescence by inducing autophagy via the mitochondrial route in human nucleus pulposus cells

Weiwei Yi, Haiyang Lan, Yafeng Wen, Yiyang Wang, Danshuang He, Zhibiao Bai, Ye Zhang, Wei Jiang, Bo Liu, Jieliang Shen, Zhenming Hu

2020Journal of Cellular Physiology22 citationsDOI

Abstract

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.

Topics & Concepts

AutophagyCell biologySenescenceMitochondrionApoptosisProgrammed cell deathCellChemistryBiologyBiochemistrySpinal Cord Injury ResearchSpine and Intervertebral Disc PathologyHeme Oxygenase-1 and Carbon Monoxide
<i>Retracted</i>: HO‐1 overexpression alleviates senescence by inducing autophagy via the mitochondrial route in human nucleus pulposus cells | Litcius