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RESEARCH PAPER / 2024-11-28

Multimorbidity is associated with myocardial DNA damage, nucleolar stress, dysregulated energy metabolism, and senescence in cardiovascular disease.

Kristina Tomkova, Marius Roman, Adewale S Adebayo, Sophia Sheikh, Syabira Yusoff, Melanie Gulston, Lathishia Joel-David, Florence Y Lai, Antonio Murgia, Bryony Eagle-Hemming, Hardeep Aujla, Tom Chad, Gavin D Richardson, Julian L Griffin, Gavin J Murphy, Marcin J Woźniak

Department of Cardiovascular Sciences and NIHR Cardiovascular Biomedical Research Unit, University of Leicester, Glenfield Hospital, Leicester, UK.Department of Cardiovascular Sciences and NIHR Cardiovascular Biomedical Research Unit, University of Leicester, Glenfield Hospital, Leicester, UK. · pubmed

Abstract

This study investigates why individuals with multimorbidity-two or more chronic conditions-are more prone to adverse outcomes after surgery. In our cohort, ninety-eight of 144 participants had multimorbidity. The myocardial transcriptome and metabolites involved in energy production were measured in 53 and 57 sequential participants, respectively. Untargeted analysis of the metabolome in blood and myocardium was performed in 30 sequential participants. Mitochondrial respiration in circulating mononuclear cells was measured in 70 participants. Results highlighted four main biological processes associated with multimorbidity: DNA damage with epigenetic changes, mitochondrial energy disruption, cellular aging (senescence) and innate immune response. Histone 2B, its ubiquitination enzymes and AKT3 were upregulated in the multimorbid group. Plasma senescence-associated proteins (IL-1β, GM-CSF) increased with more comorbidities. DNA damage and nucleolar instability were specifically apparent in multimorbid myocardium. We conclude that multimorbidity in cardiovascular patients accelerates biological aging, making them more vulnerable to metabolic stress.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper addresses the biological mechanisms underlying multimorbidity in cardiovascular disease, linking it to processes such as DNA damage, mitochondrial dysfunction, and cellular senescence. These factors are indeed relevant to the study of aging and age-related diseases, as they explore the root causes of accelerated biological aging in individuals with multiple chronic conditions. However, while the findings contribute to our understanding of these mechanisms, they do not present a significant breakthrough or transformative insights that would greatly advance the field of longevity research. Thus, the impact is rated as solid but limited.

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