Related Experiment Video
Updated: Aug 26, 2025
Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
MicroRNAs: Potential mediators between particulate matter 2.5 and Th17/Treg immune disorder in primary membranous
Xiaoshan Zhou1,2, Haoran Dai3, Hanxue Jiang1
1Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, China.
Abstract:
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.
Insights
Fine air pollutant particulate matter 2.5 (PM2.5) exposure may increase primary membranous nephropathy (PMN) risk by disrupting immune balance. PM2.5 may induce Th17/Treg imbalance via microRNAs, affecting PMN pathogenesis.
Area of Science:
- Nephrology
- Environmental Health
- Immunology
Background:
- Primary membranous nephropathy (PMN) is a leading cause of nephrotic syndrome in adults.
- Increasing PMN incidence correlates with exposure to fine particulate matter 2.5 (PM2.5).
- PM2.5 exposure may link to PMN-specific autoantigens like PLA2R1.
Purpose of the Study:
- To elucidate the molecular mechanisms linking PM2.5 exposure to PMN.
- To explore the role of Th17/Treg immune balance and microRNAs in PM2.5-induced PMN.
- To discuss PM2.5's effect on PLA2R1 exposure and PMN pathogenesis.
Main Methods:
- Review of current literature on PM2.5, PMN, Th17/Treg balance, and microRNAs.
- Analysis of potential pathways involving environmental factors, immune responses, and epigenetic modifications.
- Focus on the intermediary role of microRNAs in PM2.5-mediated immune dysregulation.
Main Results:
- PM2.5 exposure is associated with Th17/Treg immune imbalance.
- MicroRNAs may act as mediators linking PM2.5 exposure to Th17/Treg imbalance and epigenetic changes.
- PM2.5 may promote PLA2R1 exposure, contributing to PMN pathogenesis.
Conclusions:
- PM2.5 exposure potentially contributes to PMN development and progression through immune dysregulation.
- MicroRNAs play a crucial role in mediating the effects of PM2.5 on the immune system in PMN.
- Understanding these mechanisms offers new avenues for PMN prevention and treatment.
