MicroRNAs: Potential mediators between particulate matter 2.5 and Th17/Treg immune disorder in primary membranous nephropathy
Primary membranous nephropathy (PMN), is an autoimmune glomerular disease and the main reason of nephrotic syndrome in adults. Studies have confirmed that the incidence of PMN increases yearly and is related to fine air pollutants particulate matter 2.5 (PM2.5) exposure. These imply that PM2.5 may b...
| Main Authors: | , , , , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2022-09-01
|
| Series: | Frontiers in Pharmacology |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fphar.2022.968256/full |
| _version_ | 1797893967723888640 |
|---|---|
| author | Xiaoshan Zhou Xiaoshan Zhou Haoran Dai Hanxue Jiang Hongliang Rui Hongliang Rui Wenbin Liu Zhaocheng Dong Na Zhang Qihan Zhao Qihan Zhao Zhendong Feng Yuehong Hu Yuehong Hu Fanyu Hou Yang Zheng Baoli Liu Baoli Liu |
| author_facet | Xiaoshan Zhou Xiaoshan Zhou Haoran Dai Hanxue Jiang Hongliang Rui Hongliang Rui Wenbin Liu Zhaocheng Dong Na Zhang Qihan Zhao Qihan Zhao Zhendong Feng Yuehong Hu Yuehong Hu Fanyu Hou Yang Zheng Baoli Liu Baoli Liu |
| author_sort | Xiaoshan Zhou |
| collection | DOAJ |
| description | Primary membranous nephropathy (PMN), is an autoimmune glomerular disease and the main reason of nephrotic syndrome in adults. Studies have confirmed that the incidence of PMN increases yearly and is related to fine air pollutants particulate matter 2.5 (PM2.5) exposure. These imply that PM2.5 may be associated with exposure to PMN-specific autoantigens, such as the M-type receptor for secretory phospholipase A2 (PLA2R1). Emerging evidence indicates that Th17/Treg turns to imbalance under PM2.5 exposure, but the molecular mechanism of this process in PMN has not been elucidated. As an important indicator of immune activity in multiple diseases, Th17/Treg immune balance is sensitive to antigens and cellular microenvironment changes. These immune pathways play an essential role in the disease progression of PMN. Also, microRNAs (miRNAs) are susceptible to external environmental stimulation and play link role between the environment and immunity. The contribution of PM2.5 to PMN may induce Th17/Treg imbalance through miRNAs and then produce epigenetic affection. We summarize the pathways by which PM2.5 interferes with Th17/Treg immune balance and attempt to explore the intermediary roles of miRNAs, with a particular focus on the changes in PMN. Meanwhile, the mechanism of PM2.5 promoting PLA2R1 exposure is discussed. This review aims to clarify the potential mechanism of PM2.5 on the pathogenesis and progression of PMN and provide new insights for the prevention and treatment of the disease. |
| first_indexed | 2024-04-10T07:02:23Z |
| format | Article |
| id | doaj.art-1468adb0279b42edbdc591854dadbdf8 |
| institution | Directory Open Access Journal |
| issn | 1663-9812 |
| language | English |
| last_indexed | 2024-04-10T07:02:23Z |
| publishDate | 2022-09-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Pharmacology |
| spelling | doaj.art-1468adb0279b42edbdc591854dadbdf82023-02-27T16:52:37ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122022-09-011310.3389/fphar.2022.968256968256MicroRNAs: Potential mediators between particulate matter 2.5 and Th17/Treg immune disorder in primary membranous nephropathyXiaoshan Zhou0Xiaoshan Zhou1Haoran Dai2Hanxue Jiang3Hongliang Rui4Hongliang Rui5Wenbin Liu6Zhaocheng Dong7Na Zhang8Qihan Zhao9Qihan Zhao10Zhendong Feng11Yuehong Hu12Yuehong Hu13Fanyu Hou14Yang Zheng15Baoli Liu16Baoli Liu17Beijing University of Chinese Medicine, Beijing, ChinaBeijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, ChinaShunyi Branch, Beijing Hospital of Traditional Chinese Medicine, Beijing, ChinaBeijing University of Chinese Medicine, Beijing, ChinaBeijing University of Chinese Medicine, Beijing, ChinaBeijing Institute of Chinese Medicine, Beijing, ChinaSchool of Life Sciences, Beijing University of Chinese Medicine, Beijing, ChinaBeijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, ChinaSchool of Traditional Chinese Medicine, Capital Medical University, Beijing, ChinaBeijing University of Chinese Medicine, Beijing, ChinaSchool of Traditional Chinese Medicine, Capital Medical University, Beijing, ChinaPinggu Hospital, Beijing Hospital of Traditional Chinese Medicine, Beijing, ChinaBeijing University of Chinese Medicine, Beijing, ChinaSchool of Traditional Chinese Medicine, Capital Medical University, Beijing, ChinaSchool of Traditional Chinese Medicine, Changchun University of Chinese Medicine, Changchun, ChinaBeijing University of Chinese Medicine, Beijing, ChinaBeijing University of Chinese Medicine, Beijing, ChinaShunyi Branch, Beijing Hospital of Traditional Chinese Medicine, Beijing, ChinaPrimary membranous nephropathy (PMN), is an autoimmune glomerular disease and the main reason of nephrotic syndrome in adults. Studies have confirmed that the incidence of PMN increases yearly and is related to fine air pollutants particulate matter 2.5 (PM2.5) exposure. These imply that PM2.5 may be associated with exposure to PMN-specific autoantigens, such as the M-type receptor for secretory phospholipase A2 (PLA2R1). Emerging evidence indicates that Th17/Treg turns to imbalance under PM2.5 exposure, but the molecular mechanism of this process in PMN has not been elucidated. As an important indicator of immune activity in multiple diseases, Th17/Treg immune balance is sensitive to antigens and cellular microenvironment changes. These immune pathways play an essential role in the disease progression of PMN. Also, microRNAs (miRNAs) are susceptible to external environmental stimulation and play link role between the environment and immunity. The contribution of PM2.5 to PMN may induce Th17/Treg imbalance through miRNAs and then produce epigenetic affection. We summarize the pathways by which PM2.5 interferes with Th17/Treg immune balance and attempt to explore the intermediary roles of miRNAs, with a particular focus on the changes in PMN. Meanwhile, the mechanism of PM2.5 promoting PLA2R1 exposure is discussed. This review aims to clarify the potential mechanism of PM2.5 on the pathogenesis and progression of PMN and provide new insights for the prevention and treatment of the disease.https://www.frontiersin.org/articles/10.3389/fphar.2022.968256/fullPM2.5PLA2R1microRNATh17/Tregprimary membranous nephropathy (PMN) |
| spellingShingle | Xiaoshan Zhou Xiaoshan Zhou Haoran Dai Hanxue Jiang Hongliang Rui Hongliang Rui Wenbin Liu Zhaocheng Dong Na Zhang Qihan Zhao Qihan Zhao Zhendong Feng Yuehong Hu Yuehong Hu Fanyu Hou Yang Zheng Baoli Liu Baoli Liu MicroRNAs: Potential mediators between particulate matter 2.5 and Th17/Treg immune disorder in primary membranous nephropathy Frontiers in Pharmacology PM2.5 PLA2R1 microRNA Th17/Treg primary membranous nephropathy (PMN) |
| title | MicroRNAs: Potential mediators between particulate matter 2.5 and Th17/Treg immune disorder in primary membranous nephropathy |
| title_full | MicroRNAs: Potential mediators between particulate matter 2.5 and Th17/Treg immune disorder in primary membranous nephropathy |
| title_fullStr | MicroRNAs: Potential mediators between particulate matter 2.5 and Th17/Treg immune disorder in primary membranous nephropathy |
| title_full_unstemmed | MicroRNAs: Potential mediators between particulate matter 2.5 and Th17/Treg immune disorder in primary membranous nephropathy |
| title_short | MicroRNAs: Potential mediators between particulate matter 2.5 and Th17/Treg immune disorder in primary membranous nephropathy |
| title_sort | micrornas potential mediators between particulate matter 2 5 and th17 treg immune disorder in primary membranous nephropathy |
| topic | PM2.5 PLA2R1 microRNA Th17/Treg primary membranous nephropathy (PMN) |
| url | https://www.frontiersin.org/articles/10.3389/fphar.2022.968256/full |
| work_keys_str_mv | AT xiaoshanzhou micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT xiaoshanzhou micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT haorandai micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT hanxuejiang micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT hongliangrui micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT hongliangrui micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT wenbinliu micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT zhaochengdong micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT nazhang micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT qihanzhao micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT qihanzhao micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT zhendongfeng micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT yuehonghu micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT yuehonghu micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT fanyuhou micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT yangzheng micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT baoliliu micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy AT baoliliu micrornaspotentialmediatorsbetweenparticulatematter25andth17tregimmunedisorderinprimarymembranousnephropathy |