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MG53 suppresses NF-κB activation to mitigate age-related heart failure
Xiaoliang Wang, … , Chuanxi Cai, Jianjie Ma
Xiaoliang Wang, … , Chuanxi Cai, Jianjie Ma
Published July 22, 2021
Citation Information: JCI Insight. 2021;6(17):e148375. https://doi.org/10.1172/jci.insight.148375.
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Research Article Aging Cardiology

MG53 suppresses NF-κB activation to mitigate age-related heart failure

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Abstract

Aging is associated with chronic oxidative stress and inflammation that affect tissue repair and regeneration capacity. MG53 is a TRIM family protein that facilitates repair of cell membrane injury in a redox-dependent manner. Here, we demonstrate that the expression of MG53 was reduced in failing human hearts and aged mouse hearts, concomitant with elevated NF-κB activation. We evaluated the safety and efficacy of longitudinal, systemic administration of recombinant human MG53 (rhMG53) protein in aged mice. Echocardiography and pressure-volume loop measurements revealed beneficial effects of rhMG53 treatment in improving heart function of aged mice. Biochemical and histological studies demonstrated that the cardioprotective effects of rhMG53 are linked to suppression of NF-κB–mediated inflammation, reducing apoptotic cell death and oxidative stress in the aged heart. Repetitive administration of rhMG53 in aged mice did not have adverse effects on major vital organ functions. These findings support the therapeutic value of rhMG53 in treating age-related decline in cardiac function.

Authors

Xiaoliang Wang, Xiuchun Li, Hannah Ong, Tao Tan, Ki Ho Park, Zehua Bian, Xunchang Zou, Erin Haggard, Paul M. Janssen, Robert E. Merritt, Timothy M. Pawlik, Bryan A. Whitson, Nahush A. Mokadam, Lei Cao, Hua Zhu, Chuanxi Cai, Jianjie Ma

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Demographic information for the patients without failing heart (NFH) or ...

Demographic information for the patients without failing heart (NFH) or with failing heart (FH)


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