Abstract
Acute pancreatitis (AP) is a common disorder with significant hospital admission and mortality. Due to the unclarified pathological mechanism, there is still no effective and specific treatment for AP. Recently, autophagy has been found to be closely related with occurrence and development of AP, which is crucial in determining its severity and outcomes. Emerging evidence indicates that autophagy can be regulated and influenced by microRNAs and organelles, including mitochondria, endoplasmic reticulum and lysosome, through various ways in AP. Of note, the complex interplays and close relationships among autophagy, microRNA and organelles in AP are vital for figuring out pathogenesis but not clear yet. Thus, this review summarizes the role of autophagy in the pathological mechanism of AP, especially the relationship between impaired autophagy and organelles, and discusses the regulatory mechanism of microRNA on autophagy, which could offer new insights into understanding the pathogenesis of AP and developing new potential therapeutic targets against AP.
Highlights
Acute pancreatitis (AP), characterized by an inflammatory disorder of the pancreas, is the second highest cause of total hospital stays, the largest contributor to aggregate costs, and the fifth leading cause of in-hospital deaths [1], with increasing global incidence [2]
Due to the importance of microRNA in regulating human physiological and pathological processes, we discuss the regulatory mechanism of microRNA on autophagy. miRNA regulation on autophagy and the interactions between organelles and autophagy regulation are important to understand the pathogenesis of AP and offer new insights into developing new potential therapeutic targets against AP
Based on the above analysis, we can confirm that the relationships between autophagy and organelles are complicated and affected mutually; and miRNAs can regulate autophagy in AP though various pathways (Figure 1)
Summary
Acute pancreatitis (AP), characterized by an inflammatory disorder of the pancreas, is the second highest cause of total hospital stays, the largest contributor to aggregate costs, and the fifth leading cause of in-hospital deaths [1], with increasing global incidence [2]. Macroautophagy, being most widely studied, is the main form of autophagy, including in AP It starts from the formation and elongation of the membrane, and turns to be the double membrane autophagosomes, which sequester. When normal progress of autophagy is impaired, there will be accumulation of autophagic vesicles in the cytoplasm, which damage cell homeostasis and contribute to a variety of pathological states [7, 8, 11, 12]. This review summarizes the role of autophagy in the pathological mechanism of AP, especially the relationship between impaired autophagy and organelles. Due to the importance of microRNA (miRNA) in regulating human physiological and pathological processes, we discuss the regulatory mechanism of microRNA on autophagy. miRNA regulation on autophagy and the interactions between organelles and autophagy regulation are important to understand the pathogenesis of AP and offer new insights into developing new potential therapeutic targets against AP
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