Traumatic brain injury impairs cardiac function independent of chronic cerebral hypoperfusion

American Journal of Physiology-Heart and Circulatory Physiology 2026 Open access

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Authors: Claymore T. Gumbo, Deborah Corbin, Ning Zhang, Sarah L. McLaughlin, Sakthijothi Muthu, Sundararajan Venkatesh, Kate Karelina, Zachary M. Weil
DOI: 10.1152/ajpheart.00813.2025
Cited by: 1
References: 55

Abstract

TBI impairs cardiac function and induces glial activation in the insular cortex, a key autonomic region. Although mild-to-moderate chronic cerebral hypoperfusion (BCAS) induces gliosis and reduces cerebrovascular reserve, it does not exacerbate TBI-related cardiac dysfunction. Our findings demonstrate that TBI-driven neuroinflammatory signaling, rather than chronic hypoperfusion, underlies cardiac vulnerability after brain injury, highlighting the brain-heart axis as a key contributor to cardiovascular morbidity.

Fields of Study & Subjects

Neuroinflammation and Neurodegeneration Mechanisms Traumatic Brain Injury and Neurovascular Disturbances Neurological Disease Mechanisms and Treatments

Publication details

Journal / source
American Journal of Physiology-Heart and Circulatory Physiology
Publisher
American Physiological Society
Volume
330
Issue
3
Pages
H697–H707
Publication date
28 January 2026
Language
EN