Intermediate between apoptosis and necrosis, necroptosis is a regulated caspase-independent programmed cell death that induces an inflammatory response and mediates cancer development. As our understanding improves, its role in the physiopathology of numerous diseases, including pancreatic diseases, has been reconsidered, and especially in pancreatitis and pancreatic cancer. However, the exact pathogenesis remains elusive, even though some studies have been conducted on these diseases. Its unique mechanisms of action in diseases are expected to bring prospects for the treatment of pancreatic diseases. Therefore, it is imperative to further explore its molecular mechanism in pancreatic diseases in order to identify novel therapeutic options. This article introduces recent related research on necroptosis and pancreatic diseases, explores necroptosis-related molecular pathways, and provides a theoretical foundation for new therapeutic targets for pancreatic diseases.
Endothelial cells, which are highly dynamic cells essential to the vascular network, play an indispensable role in maintaining the normal function of the body. Several lines of evidence indicate that the phenotype associated with senescent endothelial cells causes or promotes some neurological disorders. In this review, we first discuss the phenotypic changes associated with endothelial cell senescence; subsequently, we provide an overview of the molecular mechanisms of endothelial cell senescence and its relationship with neurological disorders. For refractory neurological diseases such as stroke and atherosclerosis, we intend to provide some valid clues and new directions for clinical treatment options.
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