Related Experiment Video
Updated: Aug 19, 2026

Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model
Published on: November 29, 2024
TNF Receptor 1/2 Predict Heart Failure Risk in Type 2 Diabetes Mellitus Patients
Zhang Ping1, Ma Aiqun, Li Jiwu
1Department of Geriatrics and Neurology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University.
Abstract:
Inflammation plays an important role in heart failure and diabetes mellitus. Traditional serum markers have limited predictive value in heart failure and diabetes. TNFR1 and TNFR2 (TNFR1/2) have been proven to be strongly associated with heart failure and diabetes complications. This study aimed to assess the association of sTNFR1 and sTNFR2 levels and incidental HF risk in diabetes patients.We detected the mRNA, protein, and serum expression of TNFR1/2, their downstream signaling pathway protein NF-kB, and JNK expression and some traditional serum inflammatory markers in a heart failure group without diabetes mellitus or abnormal glucose tolerance (n = 84), a diabetes mellitus group without heart failure (n = 86), and a heart failure with diabetes mellitus group (n = 86).TNFR1/2 were significantly higher in patients with heart failure and diabetes mellitus based on mRNA expression to protein expression and serum expression. However, there were no differences in mRNA, protein, and serum levels of TNFR1/2 between the HF group and DM group. Furthermore, there were no differences between the groups in some traditional serum inflammatory markers.This study demonstrated higher expressions of TNFR, NF-kB, and JNK in patients with heart failure and diabetes mellitus. Compared with traditional serum markers, TNFR1 and TNFR2 are associated with heart failure risk in type 2 diabetes mellitus patients.
Related Concept Videos
Heart Failure I: Introduction
Heart Failure II: Pathophysiology
Heart Failure IV: Classification and Diagnostic Evaluation
Heart Failure V: Medical Management
Type II Diabetes I: Introduction
Type II Diabetes II: Pathophysiology