# Lnc-PFAR and autophagy in chronic pancreatitis

## TL;DR

This paper shows that lnc-PFAR, a long non-coding RNA, plays a role in autophagy and pancreatic fibrosis, suggesting a new biomarker and therapeutic target for chronic pancreatitis.

## Contribution

The study identifies a novel lnc-PFAR-pre-MIR141-RB1CC1 axis in autophagy and pancreatic fibrosis.

## Key findings

- lnc-PFAR is upregulated in human chronic pancreatitis tissues and mouse models.
- lnc-PFAR suppresses MIR141 maturation, leading to autophagy activation via RB1CC1.
- lnc-PFAR is proposed as a pharmacogenomic biomarker for pancreatic fibrosis.

## Abstract

Dysfunction of macroautophagy/autophagy has been demonstrated to contribute to multiple fibrotic diseases. In a recent study, we show that lnc-PFAR, a fibrotic-related lncRNA, is upregulated in human chronic pancreatitis tissues and mouse models and can serve as a biomarker for pancreatic fibrosis detection in the clinic. Indeed, our data reveal that lnc-PFAR affects autophagy activation through controlling MIR141 maturation. Furthermore, lnc-PFAR binds with pre-MIR141 and suppresses MIR141 maturation, which releases RB1CC1 and induces autophagy activation. We address a novel perspective of lnc-PFAR-pre-MIR141-RB1CC1 axis in autophagy and pancreatic fibrosis, and discover a prospective pharmacogenomic biomarker for chronic pancreatitis. Our findings identify a potential therapeutic target in pancreatic fibrosis and provide more evidence to consider autophagy inhibitors for further application.