Ferritinophagy: A new idea for liver diseases regulated by ferroptosis.

BACKGROUND: The discovery of regulatory cell death has led to a breakthrough in the therapeutic field. Various forms of cell death, such as necrosis, apoptosis, pyroptosis, autophagy, and ferroptosis, play an important role in the development of liver diseases. In general, more than one form of cell death pathways is responsible for the disease state. Therefore, it is particularly important to study the regulation and interaction of various cell death forms in liver diseases. DATA SOURCES: We performed a PubMed search up to November 2022 with the following keywords: ferritinophagy, ferroptosis, and liver disease. We also used terms such as signal path, inducer, and inhibitor to supplement the query results. RESULTS: This review summarized the basic characteristics of ferritinophagy and ferroptosis and the regulation of ferroptosis by ferritinophagy and reviewed the key targets and treatment strategies of ferroptosis in different liver diseases. CONCLUSIONS: Ferritinophagy is a potential therapeutic target in ferroptosis-related liver diseases.

T lymphocyte-mediated pyroptosis: A new regulatory mechanism in non-viral liver disease.

T lymphocyte-mediated pyroptosis plays an important role in the development of non-viral liver diseases. Pyroptosis as a programmed cell death process, has been a hot topic of research on disease pathogenesis in recent years. As one of the most common immune cells in the body, T cells are the major players in adaptive immunity. An increasing number of studies have shown that T lymphocyte-mediated pyroptosis functions in non-viral liver diseases to regulate immune function, alter the immune microenvironment, and thus influence disease progression. These findings will guide us and provide new ideas for the development of subsequent therapeutic agents for non-viral liver diseases.

CTRP13 attenuates the expression of LN and CAV-1 Induced by high glucose via CaMKKß/AMPK pathway in rLSECs.

OBJECTIVE: To investigate the effect and mechanism of CTRP13 on hepatic sinusoidal capillarization induced by high glucose in rat liver sinusoidal endothelial cells (rLSECs). RESULTS: CTRP13 was reduced in high glucose-treated rLSECs. High glucose increased LN and CAV-1 expression and inhibited CaMKKß and AMPK phosphorylation. CTRP13 overexpression protected rLSECs against high glucose-induced increase of LN and CAV-1 expression. Moreover, CTRP13 overexpression increased high glucose-induced inhibition of CaMKKß and AMPK activation in CTRP13-overexpressing rLSECs. Inhibition of CaMKKß and AMPK disturbed the protective effects of CTRP13 in high glucose-induced increase of LN and CAV-1. Hepatic steatosis was enhanced and basement membrane was thickened in liver of diabetic fatty liver rats. CONCLUSIONS: Our data identified the protective role of CTRP13 in hepatic sinusoidal capillarization induced by high glucose via activating CAMKKß/AMPK pathway. CTRP13 may be a potential target for screening and treating diabetic fatty liver. METHODS: Construct lentiviral CTRP13 overexpression vector and transfect rLSECs. Use STO-609 (a CaMKKß inhibitor) or Compound C (an AMPK inhibitor) to treat rLSECs. CTRP13, CaMKKß, AMPK, laminin (LN) and caveolin-1 (CAV-1) were detected by qRT-PCR and Western blotting. Establish rat model of diabetic fatty liver. Use immunohistochemistry, hematoxylin-eosin and silver staining to observe the histopathological features of liver.