Integrative transcriptomic profiling links telomere dysfunction to cGAS-STING activation in heart failure signatures in mice and humans.

Moritz Brandt, Sana'a Khraisat, Qi Luo, Megan Mayerle, Uwe Raaz, Phil Tsao, Thomas Münzel, Philipp Lurz, Philip Wenzel, Helen M Blau

Department of Cardiology, University Medical Center Mainz, Germany.Department of Cardiology, University Medical Center Mainz, Germany. · pubmed

Paper

Abstract

Cardiomyocyte telomere shortening is evident during heart failure pathogenesis. Conversely, mice with engineered telomerase deficiency develop myocardial dysfunction accompanied by p53 activation and mitochondrial repression. Yet, critical aspects remain to be established: whether cardiac dysfunction in mice lacking telomerase components arises from myocardial-intrinsic effects or systemic consequences of telomere shortening, which broader transcriptional programs follow cardiomyocyte telomere shortening, and what implications these carry for clinical heart failure.

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Research summary

The paper claims that telomere dysfunction in cardiomyocytes activates the cGAS-STING pathway, contributing to heart failure. This research is relevant as it explores the underlying mechanisms of telomere shortening, which is a fundamental aspect of aging and its associated diseases, potentially offering insights into longevity and age-related cardiac dysfunction.

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