, therefore decreased transaminase level in serum and relieved liver fibrosis in BDL mice. Besides, increased autophagy level in turn upregulated the expression of HO-1 by p62 degradation of Keap1 and subsequent activation of Nrf2 pathway. Collectively, these results indicate that HO-1 reduces gut permeability by enhancing autophagy level in CSLD, the increased autophagy establishes a HO-1-p62-Nrf2 positive feedback loop to further improve gut-liver axis disruption. Therefore, our study confirms the critical role of autophagy in HO-1 ameliorating gut-liver axis injury during CSLD, highlighting HO-1 as a promising therapeutic target.
Keyphrases
- oxidative stress
- cell death
- pi k akt
- signaling pathway
- endoplasmic reticulum stress
- liver fibrosis
- diabetic rats
- endothelial cells
- poor prognosis
- transcription factor
- liver injury
- drug induced
- cell proliferation
- metabolic syndrome
- high glucose
- long non coding rna
- adipose tissue
- sensitive detection
- fluorescent probe
- stress induced