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

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.

Quercetin Alleviates the Accumulation of Superoxide in Sodium Iodate-Induced Retinal Autophagy by Regulating Mitochondrial Reactive Oxygen Species Homeostasis through Enhanced Deacetyl-SOD2 via the Nrf2-PGC-1α-Sirt1 Pathway

“…Autophagy has been reported to be involved in the oxidative responses of age-related eye diseases [21]. An increased level of oxidative stress has been shown to contribute to various autophagy-associated proteins, such as Beclin-1, Bcl-2, LC3B, and p62 [38,42]. Beclin- Li et al reported that SOD2, an important mitochondrial oxidative scavenger, plays a key role in the regulation of mtROS, and that SOD2 activity is tightly related with acetylation at its lysine residues [32].…”

“…Autophagy has been reported to be involved in the oxidative responses of age-related eye diseases [21]. An increased level of oxidative stress has been shown to contribute to various autophagy-associated proteins, such as Beclin-1, Bcl-2, LC3B, and p62 [38,42]. Beclin-1 as a key autophagy inducer in mammalian cells can promote the formation of autophagosomes [43].…”

Single‐cell RNA‐sequencing atlas of bovine caudal intervertebral discs: Discovery of heterogeneous cell populations with distinct roles in homeostasis

“…NP4 cells also overexpress CHI3L and HMOX1, which are considered to be protective against oxidative stress-induced catabolism of the NP in the context of IVD degeneration. 94,95 Cells in oAF1 expressed a myriad of genes related to cellular stress pathways, including GADD45A, GADD45B, 86 UBB, 96 FOS, JUN, JUNB, 97 ID2, ID3, 98 MT2A, and MT1A. 99 Studies investigating the Fos/Jun signaling pathway in the IVD found opposing effects on IVD degeneration depending on which pathway activated it.…”

Nampt promotes fibroblast extracellular matrix degradation in stress urinary incontinence by inhibiting autophagy

“…The self-degradation mechanism of autophagy is involved in various pathologies by virtue of catalyzing aging cell loss and eliminating surplus or injured genes [ 46 ]. In addition, autophagy was previously associated with limited ECM production and promoted anti-senescent function in intervertebral disc degeneration [ 47 ]. Accordingly, we explored the mechanism underlying Nampt-regulation of autophagy in SUI fibroblasts, and discovered that Nampt silencing resulted in improved autophagy as evidenced by elevated LC3 II/I ratio and Beclin-1 expression levels.…”