Evidence map›Paper›PMID 41593797›Full record

ArticleDiabetology & metabolic syndrome2026

miR-4687-5p promotes the progression of diabetic retinopathy by targeting SIRT2 to mediate inflammatory responses.

Yuanlong Zhang, Sui Liu, Lichun Wei, Yanyan Cui

Abstract read
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Article in Diabetology & metabolic syndrome, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

4 authors.

Yuanlong Zhang *Integrated Traditional Chinese and Western Medicine Ophthalmology, Tianjin Eye Hospital, Tianjin, 300020, China.
Sui Liu *Department of Ophthalmology, Qingdao Municipal Hospital, Qingdao, 266011, China.
Lichun WeiDepartment of Ophthalmology II, The First People's Hospital of Lanzhou City, Lanzhou, 730050, China.
Yanyan CuiThe Second Qilu Hospital of Shandong University, Beiyuan Street, Tianqiao District, Jinan, 250000, China. cuiyy_jnmc@163.com.

Funding

Shandong Provincial Natural Youth Science Foundation ZR2024QH122
6 · The paper itself

Abstract

aimsTo investigate the role and underlying mechanisms of miR-4687-5p in diabetic retinopathy (DR) development.

methodsA total of 180 DR patients were enrolled and stratified into non-proliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR) groups. Concurrently, 100 type 2 diabetes mellitus (T2DM) patients and 100 healthy volunteers were recruited as control groups. DR cellular models were established by treating ARPE-19 cells with high glucose (HG). Reverse transcription quantitative polymerase chain reaction was used to detect gene expression. An in vitro DR cell model was constructed to explore the potential mechanism of miR-4867-5p in DR.

resultsSerum miR-4687-5p expression was significantly elevated in DR patients compared to healthy controls and T2DM patients, with the highest levels observed in PDR patients. This miRNA exhibited excellent diagnostic value for DR. miR-4687-5p expression positively correlated with clinical parameters and pro-inflammatory cytokines in DR patients. In DR cell models, miR-4687-5p overexpression inhibited cell viability, promoted apoptosis, and exacerbated inflammatory responses, whereas miR-4687-5p knockdown exerted opposite effects. Mechanistically, miR-4687-5p contributes to DR progression by negatively regulating SIRT2 to modulate cell function and inflammation.

conclusionsmiR-4687-5p is expected to become a biomarker for the early diagnosis of DR and a potential therapeutic target.

Indexed as

DiagnosisDRInflammationmiR-4687-5p

Identifiers

PMID41593797
PMCPMC12918071

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