miRNA调控原发性干燥综合征的作用机制研究进展

doi:10.12092/j.issn.1009-2501.2026.08.010

中国临床药理学与治疗学 ›› 2026, Vol. 31 ›› Issue (8): 1091-1100.doi: 10.12092/j.issn.1009-2501.2026.08.010

• 综述与讲座 • 上一篇

miRNA调控原发性干燥综合征的作用机制研究进展

王成志¹^,²(), 李松伟¹^,²^,*(), 刘一帆³, 杜萌萌¹, 朱柯颖¹, 李桓¹^,²

1. 河南中医药大学第一附属医院风湿病科，郑州 450046，河南
2. 河南中医药大学第一临床医学院，郑州 450053，河南
3. 河南中医药大学第二附属医院肛肠科，郑州 450002，河南

收稿日期:2025-07-07 修回日期:2025-09-22 出版日期:2026-08-26 发布日期:2026-09-09
通讯作者: 李松伟 E-mail:1685496995@qq.com;ryanzzdx@yeah.net
作者简介:王成志，男，博士在读，主要从事中医药防治风湿免疫疾病研究。E-mail：1685496995@qq.com
基金资助:
国家自然科学基金面上项目（81874465）；国家青年科学基金项目（82405297）；中国博士后科学基金第71批面上项目（2022M711083）；中国博士后科学基金第76批面上项目（2024M763850）；国家中医药管理局科技专项课题（GZY-KJS-2025-080）；河南中医药大学研究生科研创新能力提升专项课题（2025KYCX005）；河南中医药大学第一附属医院博士科研启动金（CZ0377-14）；河南省卫生健康委国家中医药传承创新中心联合共建科研专项课题（2024ZXZX1091）

Research progress on the mechanism of miRNA in regulating primary Sjögren's syndrome

Chengzhi WANG¹^,²(), Songwei LI¹^,²^,*(), Yifan LIU³, Mengmeng DU¹, Keying ZHU¹, Huan LI¹^,²

1. Department of Rheumatology, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450046, Henan, China
2. The First Clinical College of Henan University of Chinese Medicine, Zhengzhou 450053, Henan, China
3. Department of Coloproctology, Second Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450002, Henan, China

Received:2025-07-07 Revised:2025-09-22 Online:2026-08-26 Published:2026-09-09
Contact: Songwei LI E-mail:1685496995@qq.com;ryanzzdx@yeah.net

摘要/Abstract

摘要：

原发性干燥综合征（primary Sj?gren's syndrome，pSS）是一种慢性全身性免疫疾病，其发病机制不完全清晰，当前治疗手段有限，且缺乏根治性疗法。微小RNA（miRNA）作为重要的转录后调控因子，可广泛参与pSS免疫失调、组织损伤等病理过程，为其诊断与治疗提供新的研究方向。当pSS发病时，机体内miRNA的表达会出现异常情况，而通过调控miRNA的表达，可影响pSS的预后和转归，因此miRNA被认为是抗pSS治疗的重要标靶之一。研究发现，miR-216a-3p、miR-31-5p等可通过调控NF-κB、JAK/STAT、PI3K/AKT等信号通路，调节巨噬细胞极化、细胞凋亡、Th17/Treg平衡、T/B淋巴细胞、腺体功能、Ⅰ型干扰素（IFN）反应等，进而调控pSS的发生发展。本文综述miRNA调控pSS的作用机制，为pSS防治提供思路和依据。

关键词: miRNA, 原发性干燥综合征, 作用机制, 研究进展

Abstract:

Primary Sj?gren's syndrome (pSS) is a chronic systemic autoimmune disorder whose pathogenesis remains incompletely understood. The current treatment options are limited and there is no curative therapy. microRNA (miRNA), as important post-transcriptional regulatory factors, can widely participate in the pathological processes such as immune dysregulation and tissue damage in pSS, providing new research directions for its diagnosis and treatment. When pSS occurs, the expression of miRNAs in the body will be abnormal. By regulating the expression of miRNAs, it can affect the prognosis and outcome of pSS. Therefore, miRNAs are considered as an important target for anti-pSS treatment. Studies have found that miR-216a-3p, miR-31-5p, etc., can regulate the polarization of macrophages, cell apoptosis, Th17/Treg balance, T/B lymphocytes, glandular function, and type I IFN response through regulating the NF-κB, JAK/STAT, and PI3K/AKT signaling pathways, thereby regulating the occurrence and development of pSS. This article reviews the regulatory mechanisms of miRNAs on pSS, with the aim of providing ideas and basis for the prevention and treatment of pSS.

Key words: miRNA, primary Sj?gren's syndrome, mechanism of action, research progress

中图分类号:

R593.2

王成志, 李松伟, 刘一帆, 杜萌萌, 朱柯颖, 李桓. miRNA调控原发性干燥综合征的作用机制研究进展[J]. 中国临床药理学与治疗学, 2026, 31(8): 1091-1100.

Chengzhi WANG, Songwei LI, Yifan LIU, Mengmeng DU, Keying ZHU, Huan LI. Research progress on the mechanism of miRNA in regulating primary Sjögren's syndrome[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2026, 31(8): 1091-1100.

图/表 2

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调节机制	miRNA （表达情况）	动物模型/ 细胞模型/ 临床患者	信号通路	具体调节机制	调控pSS作用	参考文献
调节巨噬细胞极化	miR-31-5p（↑）	SS患者	p38 MAPK	NOS2、IL-1β、TNF-α↓，Arg-1、CD206、IL-10↑；M1极化↓、M2极化↑	炎症浸润、组织损伤、干眼症状↓	[11]
	miR-125b（↓）	SS小鼠	-	CD38↓，CD206↑，M2极化↑；IL-17a、IL-21↓，Th17细胞分化↓	炎症反应↓，唾液腺功能↑	[15]
	miR-100-5p（↑）	干眼症兔	-	NOS2、IRF5↓，CD206、Arg-1、KLF4↑，M2极化↑；CD4⁺Foxp3⁺Tregs↑，Tregs分化↑；TNF-α、IL-1β、IL-6↓	炎症反应、眼干程度↓	[17]
调节细胞凋亡	miR-155-5p（↓）	pSS小鼠、HSGEC细胞	PI3K/AKT	细胞凋亡↓；IL-10、IL-4↑，TNF-α、IL-6↓	炎症反应↓，腺体分泌功能↑	[19]
	miR-155-5p（↓）	SGECs细胞	NF-κB	Bax、caspase 3、caspase 9↓，Bcl-2↑，细胞凋亡↓；TNF-α、IL-6↓	炎症反应、唾液腺损伤↓	[23]
	miR-34a（↓）	NOD小鼠	NF-κB	Bcl-2↑，pro-caspase 9、caspase 9、cleaved-Caspase-3、Cyt C↓，细胞凋亡↓	唾液腺损伤↓	[25]
调节细胞凋亡	miR-223-3p（↓）	SS患者、SEGCs细胞	NF-κB	Bax、caspase-3↓，Bcl-2↑，细胞凋亡↓；IL-6、IL-12、TNF-γ↓	炎症反应↓，泪液分泌↑	[26]
调节细胞凋亡	miR-1207-5p、 miR-4695-3p（↓）	SS患者、HSG细胞	-	Bax、CASP-9、CASP-8↓，Bcl-2↑，细胞凋亡↓	唾液腺功能、唾液分泌↑	[28]
调节Th17/ Treg平衡	miRNA let-7f-5p（-）	NOD/ShiLtJ小鼠	RORC/IL-17A	CD4⁺Foxp3⁺细胞↑、CD4⁺IL-17A⁺细胞↓，Th17/Treg平衡；IL-10、TGF-β↑，IL-6、IL-17A↓	唾液分泌↑、淋巴细胞浸润↓	[31]
	miR-29a-3p（-）	NOD、Balb/c小鼠	miR-29a-3p/T-bet	Th1细胞↓，Th细胞分化↓；CD4⁺T细胞浸润↓，IFN-γ、TNF-α↓	炎症反应↓，免疫微环境、唾液分泌↑	[34]
	miR-23b-3p（↑）	NOD小鼠	NF-κB	TNF-α、IL-6、IL-17A、ING-γ↓，TGF-β1↑，Th1/Th17/Treg平衡	炎症反应↓，唾液分泌↑	[36]
	miR-146a-5p（↑）	SS患者	IL23/IL23R	ADAM17↓，IL-17A、IL-21↑，Th17细胞↑，Th17分化↑	免疫炎症反应↓	[40]
调节T/B 淋巴细胞	miR-216a-3p（-）	pSS大鼠	JAK/STAT	AFF-R、BCR、TLR-9↓，B细胞活化↓； TNF-α、IFN-γ、IL-6↓	炎症反应、组织纤维化↓、唾液分泌↑	[42]
	miR-10a-5p（-）	ESS小鼠	-	Bcl-6↓，B细胞数量、活化↓	唾液腺功能↑	[44]
	miR-125b（-）	SS患者、NOD小鼠	-	PRDM1↓，B细胞活化↓；CD19CD20CD27CD38细胞比例↓	炎症反应、腺体损伤↓，唾液流速、唾液分泌↑	[46]
	hsa-miR-30b-5p （↑）	SS患者	-	B细胞活化↓	炎症浸润↓，腺体功能↑	[48]
	hsa-miR-3202（-）	SS患者	-	MMP2↓，T细胞浸润、增殖侵袭↓	免疫炎症反应、唇腺损伤↓，腺体功能、唾液分泌↑	[49]
	miR-142-3p（↓）	SS患者	-	cAMP生成↓，钙信号↓，蛋白质生成↓；T细胞激活↑	上皮细胞功能、腺体功能↑	[53]
	miR-let-7d-3p（↑）	SS患者	AKT1/mTOR	CD4⁺T比例↓，IL-17↓	炎症反应↓	[57]
	miR-31-5p（↓）	SS患者	-	ECAR、OCR↓，葡萄糖代谢↑， T细胞反应↑	炎症反应↓	[59]
调节腺体功能	ebv-miR-BART13-3p（↓）	SS患者	-	STIM1↑、SOCE↑、钙依赖性基因↑、AQP5↑	腺体功能、唾液分泌↑	[62]
调节Ⅰ型 IFN反应	hsa-miR-145-5p（↑）	SS患者、HSG细胞	-	MUC1、TLR4、I型IFN↓	炎症反应↓，腺体功能↑	[64]
调节Ⅰ型 IFN反应	miR-744-5p（↓）	SS患者	-	PELI3↑，CCL5、CXCL10↓	炎症反应↓	[66]
调节其他机制	hsa-miR-181d-5p（↑）	SS患者	-	TNF-α介导炎症反应↓	腺体损伤↓，唾液分泌↑	[68]
调节其他机制	miR-130a、miR-708（↑）	SS患者	-	MSK1↓，cDC2激活↓，TNF-α、IL-6、 IL-12↓	炎症反应↓	[72]

调节机制	miRNA （表达情况）	动物模型/ 细胞模型/ 临床患者	信号通路	具体调节机制	调控pSS作用	参考文献
调节巨噬细胞极化	miR-31-5p（↑）	SS患者	p38 MAPK	NOS2、IL-1β、TNF-α↓，Arg-1、CD206、IL-10↑；M1极化↓、M2极化↑	炎症浸润、组织损伤、干眼症状↓	[11]
	miR-125b（↓）	SS小鼠	-	CD38↓，CD206↑，M2极化↑；IL-17a、IL-21↓，Th17细胞分化↓	炎症反应↓，唾液腺功能↑	[15]
	miR-100-5p（↑）	干眼症兔	-	NOS2、IRF5↓，CD206、Arg-1、KLF4↑，M2极化↑；CD4⁺Foxp3⁺Tregs↑，Tregs分化↑；TNF-α、IL-1β、IL-6↓	炎症反应、眼干程度↓	[17]
调节细胞凋亡	miR-155-5p（↓）	pSS小鼠、HSGEC细胞	PI3K/AKT	细胞凋亡↓；IL-10、IL-4↑，TNF-α、IL-6↓	炎症反应↓，腺体分泌功能↑	[19]
	miR-155-5p（↓）	SGECs细胞	NF-κB	Bax、caspase 3、caspase 9↓，Bcl-2↑，细胞凋亡↓；TNF-α、IL-6↓	炎症反应、唾液腺损伤↓	[23]
	miR-34a（↓）	NOD小鼠	NF-κB	Bcl-2↑，pro-caspase 9、caspase 9、cleaved-Caspase-3、Cyt C↓，细胞凋亡↓	唾液腺损伤↓	[25]
调节细胞凋亡	miR-223-3p（↓）	SS患者、SEGCs细胞	NF-κB	Bax、caspase-3↓，Bcl-2↑，细胞凋亡↓；IL-6、IL-12、TNF-γ↓	炎症反应↓，泪液分泌↑	[26]
调节细胞凋亡	miR-1207-5p、 miR-4695-3p（↓）	SS患者、HSG细胞	-	Bax、CASP-9、CASP-8↓，Bcl-2↑，细胞凋亡↓	唾液腺功能、唾液分泌↑	[28]
调节Th17/ Treg平衡	miRNA let-7f-5p（-）	NOD/ShiLtJ小鼠	RORC/IL-17A	CD4⁺Foxp3⁺细胞↑、CD4⁺IL-17A⁺细胞↓，Th17/Treg平衡；IL-10、TGF-β↑，IL-6、IL-17A↓	唾液分泌↑、淋巴细胞浸润↓	[31]
	miR-29a-3p（-）	NOD、Balb/c小鼠	miR-29a-3p/T-bet	Th1细胞↓，Th细胞分化↓；CD4⁺T细胞浸润↓，IFN-γ、TNF-α↓	炎症反应↓，免疫微环境、唾液分泌↑	[34]
	miR-23b-3p（↑）	NOD小鼠	NF-κB	TNF-α、IL-6、IL-17A、ING-γ↓，TGF-β1↑，Th1/Th17/Treg平衡	炎症反应↓，唾液分泌↑	[36]
	miR-146a-5p（↑）	SS患者	IL23/IL23R	ADAM17↓，IL-17A、IL-21↑，Th17细胞↑，Th17分化↑	免疫炎症反应↓	[40]
调节T/B 淋巴细胞	miR-216a-3p（-）	pSS大鼠	JAK/STAT	AFF-R、BCR、TLR-9↓，B细胞活化↓； TNF-α、IFN-γ、IL-6↓	炎症反应、组织纤维化↓、唾液分泌↑	[42]
	miR-10a-5p（-）	ESS小鼠	-	Bcl-6↓，B细胞数量、活化↓	唾液腺功能↑	[44]
	miR-125b（-）	SS患者、NOD小鼠	-	PRDM1↓，B细胞活化↓；CD19CD20CD27CD38细胞比例↓	炎症反应、腺体损伤↓，唾液流速、唾液分泌↑	[46]
	hsa-miR-30b-5p （↑）	SS患者	-	B细胞活化↓	炎症浸润↓，腺体功能↑	[48]
	hsa-miR-3202（-）	SS患者	-	MMP2↓，T细胞浸润、增殖侵袭↓	免疫炎症反应、唇腺损伤↓，腺体功能、唾液分泌↑	[49]
	miR-142-3p（↓）	SS患者	-	cAMP生成↓，钙信号↓，蛋白质生成↓；T细胞激活↑	上皮细胞功能、腺体功能↑	[53]
	miR-let-7d-3p（↑）	SS患者	AKT1/mTOR	CD4⁺T比例↓，IL-17↓	炎症反应↓	[57]
	miR-31-5p（↓）	SS患者	-	ECAR、OCR↓，葡萄糖代谢↑， T细胞反应↑	炎症反应↓	[59]
调节腺体功能	ebv-miR-BART13-3p（↓）	SS患者	-	STIM1↑、SOCE↑、钙依赖性基因↑、AQP5↑	腺体功能、唾液分泌↑	[62]
调节Ⅰ型 IFN反应	hsa-miR-145-5p（↑）	SS患者、HSG细胞	-	MUC1、TLR4、I型IFN↓	炎症反应↓，腺体功能↑	[64]
调节Ⅰ型 IFN反应	miR-744-5p（↓）	SS患者	-	PELI3↑，CCL5、CXCL10↓	炎症反应↓	[66]
调节其他机制	hsa-miR-181d-5p（↑）	SS患者	-	TNF-α介导炎症反应↓	腺体损伤↓，唾液分泌↑	[68]
调节其他机制	miR-130a、miR-708（↑）	SS患者	-	MSK1↓，cDC2激活↓，TNF-α、IL-6、 IL-12↓	炎症反应↓	[72]

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miRNA调控原发性干燥综合征的作用机制研究进展

Research progress on the mechanism of miRNA in regulating primary Sjögren's syndrome

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