粒体自噬
背景(考古学)
线粒体
自噬
品脱1
急性胰腺炎
机制(生物学)
胰腺炎
细胞生物学
生物
神经科学
医学
内科学
遗传学
细胞凋亡
古生物学
哲学
认识论
作者
Li Zhu,Yunfei Xu,Jian Lei
标识
DOI:10.1186/s10020-024-00903-x
摘要
Abstract Acute pancreatitis (AP) is a multifaceted inflammatory disorder stemming from the aberrant activation of trypsin within the pancreas. Despite the contribution of various factors to the pathogenesis of AP, such as trypsin activation, dysregulated increases in cytosolic Ca 2+ levels, inflammatory cascade activation, and mitochondrial dysfunction, the precise molecular mechanisms underlying the disease are still not fully understood. Mitophagy, a cellular process that preserves mitochondrial homeostasis under stress, has emerged as a pivotal player in the context of AP. Research suggests that augmenting mitophagy can mitigate pancreatic injury by clearing away malfunctioning mitochondria. Elucidating the role of mitophagy in AP may pave the way for novel therapeutic strategies. This review article aims to synthesize the current research findings on mitophagy in AP and underscore its significance in the clinical management of the disorder.
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