Abstract

Liver is a vital organ with many important functions, and the maintenance of normal hepatic function is necessary for health. As an essential mechanism for maintaining cellular homeostasis, autophagy plays an important role in ensuring normal organ function. Studies have indicated that the degeneration of hepatic function is associated with autophagic deficiency in aging liver. However, the underlying mechanisms still remain unclear. The serine protease Omi/HtrA2 belongs to the HtrA family and promotes apoptosis through either the caspase-dependent or caspase-independent pathway. Mice lacking Omi/HtrA2 exhibited progeria symptoms (premature aging), which were similar to the characteristics of autophagic insufficiency. In this study, we demonstrated that both the protein level of Omi/HtrA2 in liver and hepatic function were reduced as rats aged, and there was a positive correlation between them. Furthermore, several autophagy-related proteins (LC3II/I, Beclin-1 and LAMP2) in rat liver were decreased significantly with the increasing of age. Finally, inhibition of Omi/HtrA2 resulted in reduced autophagy and hepatic dysfunction. In conclusion, these results suggest that Omi/HtrA2 participates in age-related autophagic deficiency in rat liver. This study may offer a novel insight into the mechanism involved in liver aging.

Highlights

  • Liver is a vital organ with many important functions, and the maintenance of normal hepatic function is necessary for health

  • The results showed that the level of LC3II/I and Beclin-1 were repressed after ucf-101 treatment in liver of rats from 3 and 9-month group, implying that the autophagy level was likely to be reduced by inhibiting Omi/HtrA2 activity (Fig. 5A-B)

  • All above data indicated that inhibition of Omi/HtrA2 resulted in reduced autophagy in liver

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Summary

Introduction

Liver is a vital organ with many important functions, and the maintenance of normal hepatic function is necessary for health. Omi/HtrA2 can regulate both basal and stress-induced autophagy in neuronal cells [21], indicating that Omi/HtrA2 may be involved in autophagic deficiency of aging liver. These results indicated that the level of Omi/HtrA2 in liver showed a progressive decline with increasing age (Fig. 3A-C).

Results
Conclusion
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