Biomarkers of Immune Injury in Cardiometabolic Disorders
- 1Key Laboratory of Birth Defects and Related Diseases of Women and Children of MOE, Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu 610041, China
Abstract
Cardiometabolic disorders are accompanied by persistent immune activation that links metabolic stress to vascular and organ injury. Conventional inflammatory measures capture part of this process, but they provide limited information about tissue origin, biological mechanism and disease trajectory. This narrative review examines emerging biomarkers across genetic and epigenetic regulation, metabolic and oxidative stress, gut microbial exposure, innate immune activation, adaptive immune remodeling and circulating inflammatory responses. It integrates mechanistic studies with clinical observations to consider how these signals may inform the assessment of cardiometabolic immune injury. Particular attention is given to the distinction between inherited susceptibility and acquired responses, circulating associations and tissue mechanisms, and potentially injurious versus compensatory immune activity. The evidence supports substantial biological connectivity among these domains, while the strength of clinical validation varies widely. Most candidate markers and proposed combinations require standardized measurement, longitudinal assessment and external validation before biomarker-guided prevention can be justified. We propose a mechanism-informed framework for organizing candidate immune-metabolic phenotypes, recognizing reciprocal interactions rather than a universal temporal sequence. Future studies should determine whether these biomarkers improve prediction and clinical decisions beyond established risk factors and whether changes in biomarker profiles correspond to meaningful treatment benefits.
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BibTeX
@article{zhou2026biomarkers,
title = {{Biomarkers of Immune Injury in Cardiometabolic Disorders}},
author = {Letao Zhou and Yifei Li},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = nov,
doi = {10.3390/ijms27219913},
url = {https://www.mdpi.com/1422-0067/27/21/9913},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Biomarkers of Immune Injury in Cardiometabolic Disorders
AU - Letao Zhou
AU - Yifei Li
PY - 2026
DA - 2026/11/05
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219913
UR - https://www.mdpi.com/1422-0067/27/21/9913
AB - Cardiometabolic disorders are accompanied by persistent immune activation that links metabolic stress to vascular and organ injury. Conventional inflammatory measures capture part of this process, but they provide limited information about tissue origin, biological mechanism and disease trajectory. This narrative review examines emerging biomarkers across genetic and epigenetic regulation, metabolic and oxidative stress, gut microbial exposure, innate immune activation, adaptive immune remodeling and circulating inflammatory responses. It integrates mechanistic studies with clinical observations to consider how these signals may inform the assessment of cardiometabolic immune injury. Particular attention is given to the distinction between inherited susceptibility and acquired responses, circulating associations and tissue mechanisms, and potentially injurious versus compensatory immune activity. The evidence supports substantial biological connectivity among these domains, while the strength of clinical validation varies widely. Most candidate markers and proposed combinations require standardized measurement, longitudinal assessment and external validation before biomarker-guided prevention can be justified. We propose a mechanism-informed framework for organizing candidate immune-metabolic phenotypes, recognizing reciprocal interactions rather than a universal temporal sequence. Future studies should determine whether these biomarkers improve prediction and clinical decisions beyond established risk factors and whether changes in biomarker profiles correspond to meaningful treatment benefits.
SN - 1422-0067
ER -