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The Mechanism of Lung and Intestinal Injury in Acute Pancreatitis: A Review
Acute pancreatitis (AP), as a common cause of clinical acute abdomen, often leads to multi-organ damage. In the process of severe AP, the lungs and intestines are the most easily affected organs aside the pancreas. These organ damages occur in succession. Notably, lung and intestinal injuries are cl...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9301017/ https://www.ncbi.nlm.nih.gov/pubmed/35872761 http://dx.doi.org/10.3389/fmed.2022.904078 |
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author | Liu, Dongling Wen, Linlin Wang, Zhandong Hai, Yang Yang, Dan Zhang, Yanying Bai, Min Song, Bing Wang, Yongfeng |
author_facet | Liu, Dongling Wen, Linlin Wang, Zhandong Hai, Yang Yang, Dan Zhang, Yanying Bai, Min Song, Bing Wang, Yongfeng |
author_sort | Liu, Dongling |
collection | PubMed |
description | Acute pancreatitis (AP), as a common cause of clinical acute abdomen, often leads to multi-organ damage. In the process of severe AP, the lungs and intestines are the most easily affected organs aside the pancreas. These organ damages occur in succession. Notably, lung and intestinal injuries are closely linked. Damage to ML, which transports immune cells, intestinal fluid, chyle, and toxic components (including toxins, trypsin, and activated cytokines to the systemic circulation in AP) may be connected to AP. This process can lead to the pathological changes of hyperosmotic edema of the lung, an increase in alveolar fluid level, destruction of the intestinal mucosal structure, and impairment of intestinal mucosal permeability. The underlying mechanisms of the correlation between lung and intestinal injuries are inflammatory response, oxidative stress, and endocrine hormone secretion disorders. The main signaling pathways of lung and intestinal injuries are TNF-α, HMGB1-mediated inflammation amplification effect of NF-κB signal pathway, Nrf2/ARE oxidative stress response signaling pathway, and IL-6-mediated JAK2/STAT3 signaling pathway. These pathways exert anti-inflammatory response and anti-oxidative stress, inhibit cell proliferation, and promote apoptosis. The interaction is consistent with the traditional Chinese medicine theory of the lung being connected with the large intestine (fei yu da chang xiang biao li in Chinese). This review sought to explore intersecting mechanisms of lung and intestinal injuries in AP to develop new treatment strategies. |
format | Online Article Text |
id | pubmed-9301017 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-93010172022-07-22 The Mechanism of Lung and Intestinal Injury in Acute Pancreatitis: A Review Liu, Dongling Wen, Linlin Wang, Zhandong Hai, Yang Yang, Dan Zhang, Yanying Bai, Min Song, Bing Wang, Yongfeng Front Med (Lausanne) Medicine Acute pancreatitis (AP), as a common cause of clinical acute abdomen, often leads to multi-organ damage. In the process of severe AP, the lungs and intestines are the most easily affected organs aside the pancreas. These organ damages occur in succession. Notably, lung and intestinal injuries are closely linked. Damage to ML, which transports immune cells, intestinal fluid, chyle, and toxic components (including toxins, trypsin, and activated cytokines to the systemic circulation in AP) may be connected to AP. This process can lead to the pathological changes of hyperosmotic edema of the lung, an increase in alveolar fluid level, destruction of the intestinal mucosal structure, and impairment of intestinal mucosal permeability. The underlying mechanisms of the correlation between lung and intestinal injuries are inflammatory response, oxidative stress, and endocrine hormone secretion disorders. The main signaling pathways of lung and intestinal injuries are TNF-α, HMGB1-mediated inflammation amplification effect of NF-κB signal pathway, Nrf2/ARE oxidative stress response signaling pathway, and IL-6-mediated JAK2/STAT3 signaling pathway. These pathways exert anti-inflammatory response and anti-oxidative stress, inhibit cell proliferation, and promote apoptosis. The interaction is consistent with the traditional Chinese medicine theory of the lung being connected with the large intestine (fei yu da chang xiang biao li in Chinese). This review sought to explore intersecting mechanisms of lung and intestinal injuries in AP to develop new treatment strategies. Frontiers Media S.A. 2022-07-07 /pmc/articles/PMC9301017/ /pubmed/35872761 http://dx.doi.org/10.3389/fmed.2022.904078 Text en Copyright © 2022 Liu, Wen, Wang, Hai, Yang, Zhang, Bai, Song and Wang. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Medicine Liu, Dongling Wen, Linlin Wang, Zhandong Hai, Yang Yang, Dan Zhang, Yanying Bai, Min Song, Bing Wang, Yongfeng The Mechanism of Lung and Intestinal Injury in Acute Pancreatitis: A Review |
title | The Mechanism of Lung and Intestinal Injury in Acute Pancreatitis: A Review |
title_full | The Mechanism of Lung and Intestinal Injury in Acute Pancreatitis: A Review |
title_fullStr | The Mechanism of Lung and Intestinal Injury in Acute Pancreatitis: A Review |
title_full_unstemmed | The Mechanism of Lung and Intestinal Injury in Acute Pancreatitis: A Review |
title_short | The Mechanism of Lung and Intestinal Injury in Acute Pancreatitis: A Review |
title_sort | mechanism of lung and intestinal injury in acute pancreatitis: a review |
topic | Medicine |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9301017/ https://www.ncbi.nlm.nih.gov/pubmed/35872761 http://dx.doi.org/10.3389/fmed.2022.904078 |
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