Evidence map›Paper›PMID 42044916›Full record

ReviewDiabetes & metabolism journal2026

Neutrophil-Linked Inflammatory Mechanisms and Biomarkers in Diabetic Microvascular Complications.

Junseo Kim, Daeun Jung, Da Hyun Kang, Hyeongseok Kim, Junyoung O Park, Jun Young Heo, Seong Eun Lee, Hyun Jin Kim, Ju Hee Lee, Yea Eun Kang and 1 more

Abstract readReview
In one paragraph

Review in Diabetes & metabolism journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Junseo Kim *Department of Medical Science, Chungnam National University College of Medicine, Daejeon, Korea.
Daeun Jung *Chungnam National University College of Medicine, Daejeon, Korea.
Da Hyun Kang *Department of Internal Medicine, Chungnam National University College of Medicine, Daejeon, Korea.
Hyeongseok KimDepartment of Medical Science, Chungnam National University College of Medicine, Daejeon, Korea.
Junyoung O ParkDepartment of Chemical and Biomolecular Engineering, University of California, Los Angeles, Los Angeles, CA, USA.
Jun Young HeoDepartment of Medical Science, Chungnam National University College of Medicine, Daejeon, Korea.
Seong Eun LeeSystem Network Inflammation Control Research Center, Chungnam National University, Daejeon, Korea.
Hyun Jin KimDepartment of Medical Science, Chungnam National University College of Medicine, Daejeon, Korea.
Ju Hee LeeDepartment of Medical Science, Chungnam National University College of Medicine, Daejeon, Korea.
Yea Eun KangDepartment of Medical Science, Chungnam National University College of Medicine, Daejeon, Korea.
Bon Jeong KuDepartment of Medical Science, Chungnam National University College of Medicine, Daejeon, Korea.

Funding

Korea Health Industry Development InstituteMinistry of Health and Welfare RS-2020-KH088690Ministry of Health and Welfare RS-2025-24536373Ministry of Science and ICT RS-2024-00406568National Research Foundation of Korea RS-2021-NR061617
6 · The paper itself

Abstract

Diabetic microvascular complications, including nephropathy, retinopathy, and neuropathy, are major causes of morbidity in diabetes. Increasing evidence highlights neutrophils as key contributors to the chronic inflammatory processes underlying these complications. In the diabetic environment, neutrophils exhibit impaired recruitment, defective phagocytosis, dysregulated degranulation, and excessive production of reactive oxygen species and neutrophil extracellular traps (NETs). These dysfunctions not only reduce pathogen clearance but also exacerbate tissue injury through persistent low-grade inflammation. Furthermore, neutrophils interact with other immune cells, such as macrophages, dendritic cells, T cells, and B cells, perpetuating immune imbalance and tissue damage. Various neutrophil-derived cytokines and granular proteins also influence vascular permeability and endothelial dysfunction. In recent years, neutrophil-related biomarkers-such as absolute neutrophil count, neutrophil-to-lymphocyte ratio, platelet-to-neutrophil ratio, and systemic immune-inflammation index-have gained attention as accessible and cost-effective tools for predicting and monitoring diabetic microvascular complications. This review summarizes the multifaceted roles of neutrophils in the pathogenesis of diabetic microvascular disease and highlights emerging clinical applications of neutrophil-based inflammatory biomarkers. A better understanding of neutrophil-driven mechanisms may open new avenues for early diagnosis, therapeutic intervention, and personalized care in diabetic patients.

Indexed as

Diabetic AngiopathiesInflammationNeutrophilsBiomarkersDiabetes Mellitus, Type 2Diabetic NephropathiesDiabetic NeuropathiesDiabetic RetinopathyHumansBiomarkersDiabetes mellitus, type 2Diabetic nephropathiesDiabetic neuropathiesDiabetic retinopathyNeutrophils

Identifiers

PMID42044916
PMCPMC13175710

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.