Physiological Modulation of Neutrophil Activation and Recruitment by Heat Shock Protein 90 in Acute Pancreatitis
DOI:
https://doi.org/10.48047/dwnp4j05Keywords:
Amylase, Chemokines, Inflammation, Leukocytes, and PancreasAbstract
Background and Objective: Severe acute pancreatitis (AP) is characterized by leukocyte infiltration and tissue necrosis, yet the cellular signaling pathways driving pancreatic damage remain poorly understood. Heat shock protein 90 (HSP90) is a key regulator of specific cellular functions, promoting pro-inflammatory responses. This study investigates the role of HSP90 signaling in acute pancreatitis.
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References
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Wetterholm E, Linders J, Merza M, Regner S, Thorlacius H. Platelet derived CXCL4 regulates neutrophil infiltration and tissue damage in severe acute
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Dahiya DS, Jahagirdar V, Chandan S, Gangwani MK, Merza N, Ali H, et al. Acute pancreatitis in liver transplant hospitalizations: Identifying national trends, clinical outcomes and healthcare burden in the United States. World J Hepatol. 2023;15(6):797-812.
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