Association between autophagy and acute pancreatitis

Zhang, Tao; Gan, Yu; Zhu, Song

doi:10.3389/fgene.2023.998035

Cited by 9 publications

(7 citation statements)

References 85 publications

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“…Dysfunction of the autophagy process has been proven to be a key mechanism in many diseases, including cancer, inflammation, infection, degeneration, and metabolic disorders 20 . Recent studies have indicated that autophagy is one of the early events in acute pancreatitis 21 . Impaired autophagy can promote abnormal activation of zymogen granules, leading to apoptosis and necrosis of exocrine pancreatic cells 21 .…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have indicated that autophagy is one of the early events in acute pancreatitis 21 . Impaired autophagy can promote abnormal activation of zymogen granules, leading to apoptosis and necrosis of exocrine pancreatic cells 21 . Furthermore, it was found that the SQSTM1 (sequestosome 1) in the serum of AP patients is significantly increased, and additional study revealed that the intracellular SQSTM1 protein increased the expression of ACSL4 in a manner dependent on the receptor for advanced glycation end products (AGER), leading to the production of polyunsaturated fatty acids, inducing autophagosome formation, and subsequently causing ferroptosis, exacerbating the course of AP 22 .…”

Section: Discussionmentioning

confidence: 99%

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ACLS4 could be a potential therapeutic target for severe acute pancreatitis

Guo,

Lu,

et al. 2024

Sci Rep

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Acute pancreatitis (AP) is currently among the most prevalent digestive diseases. The pathogenesis of AP remains elusive, and there is no specific treatment. Therefore, identifying novel therapeutic targets is imperative for effective management and prevention of AP. In this study, we conducted a comprehensive transcriptomic analysis of peripheral blood from patients with AP and the pancreatic tissue from a mouse model of AP. Our analyses revealed that mouse model of AP exhibited a higher enrichment of mitogen-activated protein kinase signaling, endocytosis, apoptosis and tight junction pathways than the control. Subsequent weighted gene co-expression network analysis identified 15 gene modules, containing between 50 and 1000 genes each, which demonstrated significant correlations within samples from patients with AP. Further screening identified four genes (ACSL4, GALNT3, WSB1, and IL1R1) that were significantly upregulated in severe acute pancreatitis (SAP) in both human and mouse samples. In mouse models of SAP, ACSL4 was significantly upregulated in the pancreas, whereas GALNT3, WSB1, and IL1R1 were not. Lastly, we found that a commercially available ACSL4 inhibitor, PRGL493, markedly reduced IL-6 and TNFα expression, alleviated pancreatic edema and necrosis, and diminished the infiltration of inflammatory cells. In conclusion, this study comprehensively depicts the key genes and signaling pathways implicated in AP and suggests the potential of ACSL4 as a novel therapeutic target for SAP. These findings provide valuable insights for further exploration of therapeutic strategies for SAP.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

ACLS4 could be a potential therapeutic target for severe acute pancreatitis

Guo,

Lu,

et al. 2024

Sci Rep

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“…It is believed that AP may rely on the theory of the activated pathway of lysosome and autophagy ( 17 ). Naturally, the easiest pathophysiological mechanism represents ischemia of pancreatic tissue leading to dysregulated enzymatic activities ( 19 ).…”

Section: Discussionmentioning

confidence: 99%

“…In light of the role of insulin in the AP pathophysiology due to the hypertriglyceridemia state as the known risk factor for AP development, defective pancreatic cells contribute to insulin deficiency ( 15 ). Insulin is proven to decrease the hypertriglyceridemia state and in that way acts as a preventive care measure in terms of pancreatic parenchymal preservation ( 1 , 17 ).…”

Section: Discussionmentioning

confidence: 99%

Diagnostic Potential of Ratio Between Creatine Kinase and Amylase in Acute Pancreatitis

Selimovic,

Jahic,

Kurtovic

et al. 2023

Mater Sociomed

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Background: Acute pancreatitis (AP) is an acute inflammatory illness of the pancreas representing a true question in diagnostic process. Laboratory markers of the hepatobiliary tract such as liver transaminases with pancreatic enzymes give a true hint of a hidden diagnosis together with urea, creatinine and creatine kinase (CK). Objective: This clinical study aims to show whether there is any correlation between alpha-amylase and CK or their ratio examining hospitalized patients with AP diagnosis. Methods: From total number of 99 patients with a clinical picture of AP, 71 patients in this retrospective analysis (including both genders) were included according to the presence of two biochemical markers in collected laboratory analysis at admission and 72 hours later on a laboratory check-up: CK and alpha-amylase. Results: The median CK value of AP cases was 92 (41.75 – 207.25) in the acute period and 73 (37 – 159) after 72h staying in the hospital without statistical significant (p=0.521; p<0.05). However, there was a statistically significant correlation between the parameters of CK at admission and creatine kinase after 72h staying in the hospital. The median value of CK/Amylase ratio in the acute period was 0.168 (0.069 – 0.532) and 0.386 (0.12 – 1.12) after 72 hours of staying in the hospital. There was a statistically significant difference between values of CK/amylase ratio in these two groups (p=0.000; p<0.01). Conclusion: In conclusion, a connection between CK and alpha-amylase needs to be elucidated in further studies and its existence must be researched both in physiological and pathophysiological conditions, and it is two-way and very complex. This study helped us obtain significant information about the perspective of AP in the potential relation to other non-standard laboratory markers for some diseases

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“…Recurrent acute pancreatitis increases the risk of developing chronic pancreatitis, and survivors experience reduced long-term quality of life [ [17] , [18] , [19] ]. Core events in acute pancreatitis pathogenesis include pathological calcium signaling, mitochondrial dysfunction, premature activation of proteolytic enzymes, endoplasmic reticulum stress, impaired unfolded protein response, and impaired autophagy [ [20] , [21] , [22] , [24] , [25] , [26] , [27] [20–22,24–27, 23 ]. Inhibition of nuclear factor-kappaB activation, NLRP3 inhibition, restoration of mitochondrial and/or autophagic function, ORAI1 inhibition, inhibition of the RIP1-RIP3 pathway, TNF-alpha inhibition, autophagy pathway inhibition, TLR4 expression suppression, and oxidative stress inhibition have emerged as potential targets or pathways for acute pancreatitis treatment [ [28] , [29] , [30] , [31] , [32] , [33] , [34] , [35] ].…”

Section: Introductionmentioning

confidence: 99%

Research trends on traditional Chinese medicine and acute pancreatitis: A bibliometric analysis from 2007 to mid-2023

Lan,

Guo,

Zhou

et al. 2024

Heliyon

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Association between autophagy and acute pancreatitis

Cited by 9 publications

References 85 publications

ACLS4 could be a potential therapeutic target for severe acute pancreatitis

ACLS4 could be a potential therapeutic target for severe acute pancreatitis

Diagnostic Potential of Ratio Between Creatine Kinase and Amylase in Acute Pancreatitis

Research trends on traditional Chinese medicine and acute pancreatitis: A bibliometric analysis from 2007 to mid-2023

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