Non-apoptotic programmed cell deaths in diabetic pulmonary dysfunction: the new side of advanced glycation end products
Diabetes mellitus (DM) is a chronic metabolic disorder that affects multiple organs and systems, including the pulmonary system. Pulmonary dysfunction in DM patients has been observed and studied for years, but the underlying mechanisms have not been fully understood. In addition to traditional mech...
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Published in | Frontiers in endocrinology (Lausanne) Vol. 14; p. 1126661 |
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26.10.2023
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Abstract | Diabetes mellitus (DM) is a chronic metabolic disorder that affects multiple organs and systems, including the pulmonary system. Pulmonary dysfunction in DM patients has been observed and studied for years, but the underlying mechanisms have not been fully understood. In addition to traditional mechanisms such as the production and accumulation of advanced glycation end products (AGEs), angiopathy, tissue glycation, oxidative stress, and systemic inflammation, recent studies have focused on programmed cell deaths (PCDs), especially the non-apoptotic ones, in diabetic pulmonary dysfunction. Non-apoptotic PCDs (NAPCDs) including autophagic cell death, necroptosis, pyroptosis, ferroptosis, and copper-induced cell death have been found to have certain correlations with diabetes and relevant complications. The AGE–AGE receptor (RAGE) axis not only plays an important role in the traditional pathogenesis of diabetes lung disease but also plays an important role in non-apoptotic cell death. In this review, we summarize novel studies about the roles of non-apoptotic PCDs in diabetic pulmonary dysfunction and focus on their interactions with the AGE–RAGE axis. |
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AbstractList | Diabetes mellitus (DM) is a chronic metabolic disorder that affects multiple organs and systems, including the pulmonary system. Pulmonary dysfunction in DM patients has been observed and studied for years, but the underlying mechanisms have not been fully understood. In addition to traditional mechanisms such as the production and accumulation of advanced glycation end products (AGEs), angiopathy, tissue glycation, oxidative stress, and systemic inflammation, recent studies have focused on programmed cell deaths (PCDs), especially the non-apoptotic ones, in diabetic pulmonary dysfunction. Non-apoptotic PCDs (NAPCDs) including autophagic cell death, necroptosis, pyroptosis, ferroptosis, and copper-induced cell death have been found to have certain correlations with diabetes and relevant complications. The AGE–AGE receptor (RAGE) axis not only plays an important role in the traditional pathogenesis of diabetes lung disease but also plays an important role in non-apoptotic cell death. In this review, we summarize novel studies about the roles of non-apoptotic PCDs in diabetic pulmonary dysfunction and focus on their interactions with the AGE–RAGE axis. Diabetes mellitus (DM) is a chronic metabolic disorder that affects multiple organs and systems, including the pulmonary system. Pulmonary dysfunction in DM patients has been observed and studied for years, but the underlying mechanisms have not been fully understood. In addition to traditional mechanisms such as the production and accumulation of advanced glycation end products (AGEs), angiopathy, tissue glycation, oxidative stress, and systemic inflammation, recent studies have focused on programmed cell deaths (PCDs), especially the non-apoptotic ones, in diabetic pulmonary dysfunction. Non-apoptotic PCDs (NAPCDs) including autophagic cell death, necroptosis, pyroptosis, ferroptosis, and copper-induced cell death have been found to have certain correlations with diabetes and relevant complications. The AGE-AGE receptor (RAGE) axis not only plays an important role in the traditional pathogenesis of diabetes lung disease but also plays an important role in non-apoptotic cell death. In this review, we summarize novel studies about the roles of non-apoptotic PCDs in diabetic pulmonary dysfunction and focus on their interactions with the AGE-RAGE axis.Diabetes mellitus (DM) is a chronic metabolic disorder that affects multiple organs and systems, including the pulmonary system. Pulmonary dysfunction in DM patients has been observed and studied for years, but the underlying mechanisms have not been fully understood. In addition to traditional mechanisms such as the production and accumulation of advanced glycation end products (AGEs), angiopathy, tissue glycation, oxidative stress, and systemic inflammation, recent studies have focused on programmed cell deaths (PCDs), especially the non-apoptotic ones, in diabetic pulmonary dysfunction. Non-apoptotic PCDs (NAPCDs) including autophagic cell death, necroptosis, pyroptosis, ferroptosis, and copper-induced cell death have been found to have certain correlations with diabetes and relevant complications. The AGE-AGE receptor (RAGE) axis not only plays an important role in the traditional pathogenesis of diabetes lung disease but also plays an important role in non-apoptotic cell death. In this review, we summarize novel studies about the roles of non-apoptotic PCDs in diabetic pulmonary dysfunction and focus on their interactions with the AGE-RAGE axis. |
Author | Dai, Yimin Qiao, Lin Li, Mengtao Peng, Zhao Zeng, Xiaofeng Wu, Chanyuan Wang, Qian Zhou, Shuang Xu, Dong Zhao, Jiuliang |
AuthorAffiliation | Department of Rheumatology and Clinical Immunology, Chinese Academy of Medical Sciences and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases (NCRC-DID), Ministry of Science and Technology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital (PUMCH), Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education , Beijing , China |
AuthorAffiliation_xml | – name: Department of Rheumatology and Clinical Immunology, Chinese Academy of Medical Sciences and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases (NCRC-DID), Ministry of Science and Technology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital (PUMCH), Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education , Beijing , China |
Author_xml | – sequence: 1 givenname: Yimin surname: Dai fullname: Dai, Yimin – sequence: 2 givenname: Shuang surname: Zhou fullname: Zhou, Shuang – sequence: 3 givenname: Lin surname: Qiao fullname: Qiao, Lin – sequence: 4 givenname: Zhao surname: Peng fullname: Peng, Zhao – sequence: 5 givenname: Jiuliang surname: Zhao fullname: Zhao, Jiuliang – sequence: 6 givenname: Dong surname: Xu fullname: Xu, Dong – sequence: 7 givenname: Chanyuan surname: Wu fullname: Wu, Chanyuan – sequence: 8 givenname: Mengtao surname: Li fullname: Li, Mengtao – sequence: 9 givenname: Xiaofeng surname: Zeng fullname: Zeng, Xiaofeng – sequence: 10 givenname: Qian surname: Wang fullname: Wang, Qian |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37964954$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_12677_acm_2024_1482192 crossref_primary_10_1186_s10020_024_00905_9 crossref_primary_10_1007_s10557_024_07639_0 crossref_primary_10_1016_j_intimp_2024_112304 crossref_primary_10_2147_COPD_S447739 |
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Keywords | advanced glycosylation end products inflammation non-apoptotic programmed cell deaths diabetic pulmonary dysfunction oxidative stress |
Language | English |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 Reviewed by: Sichong Ren, Chengdu Medical College, China; Durai Sellegounder, Buck Institute for Research on Aging, United States These authors have contributed equally to this work and share first authorship Edited by: Xiaoqiang Tang, Sichuan University, China |
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Snippet | Diabetes mellitus (DM) is a chronic metabolic disorder that affects multiple organs and systems, including the pulmonary system. Pulmonary dysfunction in DM... |
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StartPage | 1126661 |
SubjectTerms | advanced glycosylation end products Apoptosis Autophagic Cell Death Diabetes Mellitus diabetic pulmonary dysfunction Endocrinology Glycation End Products, Advanced - metabolism Humans inflammation non-apoptotic programmed cell deaths oxidative stress Receptor for Advanced Glycation End Products - metabolism |
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Title | Non-apoptotic programmed cell deaths in diabetic pulmonary dysfunction: the new side of advanced glycation end products |
URI | https://www.ncbi.nlm.nih.gov/pubmed/37964954 https://www.proquest.com/docview/2890363122 https://pubmed.ncbi.nlm.nih.gov/PMC10641270 https://doaj.org/article/8af1ea9ee1094a569a6f6582082caee4 |
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