Related Experiment Video
Updated: Apr 30, 2026

Mouse Electroacupuncture Fixation Device Fabrication for Electroacupuncture Pretreatment in Diabetic Cardiomyopathy Mouse Model
Published on: April 18, 2025
Increased peripheral proinflammatory T helper subsets contribute to cardiovascular complications in diabetic patients
Ru-xing Zhao1, Wen-juan Li2, Yi-ran Lu2
1Department of Endocrinology, Qilu Hospital of Shandong University, Jinan 250012, China ; Institute of Endocrinology and Metabolism, Shandong University, Jinan 250012, China.
Insights
Increased proinflammatory T helper cells, particularly Th22 cells, are linked to cardiovascular complications in type 2 diabetes patients. These immune cells may serve as novel predictors for coronary heart disease risk in diabetes.
Area of Science:
- Immunology
- Cardiology
- Endocrinology
Background:
- Coronary atherosclerotic heart disease (CHD) is a significant concern for individuals with type 2 diabetes (T2D).
- Systemic chronic inflammation is hypothesized to link T2D and increased cardiovascular disease risk.
- Increased peripheral proinflammatory T helper cell subsets may contribute to cardiovascular complications in diabetic patients.
Purpose of the Study:
- To investigate the association between peripheral proinflammatory T helper cell subsets and coronary atherosclerotic heart disease (CHD) in type 2 diabetes (T2D) patients.
- To determine if specific T helper cell subsets are independent risk factors for cardiovascular complications in diabetes.
Main Methods:
- Flow cytometry was used to quantify peripheral CD4+ T helper cells, including Th1, Th17, and Th22 subsets.
- Analysis was performed on diabetic patients with and without CHD (n=42 and n=67, respectively).
- Statistical analyses included logistic regression and cross-table analysis.
Main Results:
- Diabetic patients with CHD exhibited higher frequencies and numbers of Th1, Th17, and Th22 cells compared to those without CHD.
- Increased proinflammatory T helper subsets, especially Th22, were identified as independent risk factors for cardiovascular complications in diabetes.
- Elevated Th subsets correlated with increased C-reactive protein (CRP) levels and the atherogenic index of plasma.
- Th1 frequency and Th22 numbers showed potential in predicting CHD in diabetic individuals.
Conclusions:
- Elevated peripheral proinflammatory T helper subsets contribute synergistically to the high prevalence of diabetic cardiovasculopathy.
- Th22 cells may play an independent role in CHD development and serve as a novel indicator of cardiovascular risk in diabetes.
Background:
Coronary atherosclerotic heart disease (CHD) is one of the major concerns in type 2 diabetes (T2D). The systemic chronic inflammation has been postulated to bridge the increased risk of cardiovascular disease and T2D. We formulated that increased peripheral proinflammatory T helper subsets contributed to the development of cardiovascular complications in diabetic patients.
Methods:
The frequencies of peripheral total CD4+ T helper cells, proinflammatory Th1, Th17, and Th22 subsets were determined by flow cytometry in diabetic patients with or without CHD (n = 42 and 67, resp.).
Results:
Both peripheral frequencies and total numbers of Th1, Th17, and Th22 cells were further increased in diabetic patients with CHD. Logistic regression and categorical cross-table analysis further confirmed that increased proinflammatory Th subsets, especially Th22, were independent risk factors of cardiovascular complication in diabetes. Elevated Th subsets also correlated with increased CRP levels and the atherogenic index of plasma. Moreover, Th1 frequency and Th22 numbers demonstrated remarkable potential in predicting CHD in diabetes.
Conclusions:
Increased peripheral proinflammatory T helper subsets act in concert and contribute to the increased prevalence of diabetic cardiovasculopathy. The recently identified Th22 cells might play an independent role in CHD and represent a novel proxy for cardiovascular risks in diabetes.
Related Concept Videos
Complications of Diabetes Mellitus
Type II Diabetes II: Pathophysiology
Coronary Artery Disease I: Introduction
Type I Diabetes II: Pathophysiology
Diabetic Retinopathy
Diabetic Nephropathy

