Clonal Hematopoiesis: A New Step Linking Inflammation to Heart Failure

•Clonal hematopoiesis is a common condition in the elderly that can result from the acquisition of somatic mutations in HSPCs that confer a selective advantage and allow for clonal cell expansion.•This clonal population of mutated HSPCs can give rise to leukocytes with altered immune properties, and...

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Veröffentlicht in:JACC. Basic to translational science 2020-02, Vol.5 (2), p.196-207
Hauptverfasser: Yura, Yoshimitsu, Sano, Soichi, Walsh, Kenneth
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Sprache:eng
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Zusammenfassung:•Clonal hematopoiesis is a common condition in the elderly that can result from the acquisition of somatic mutations in HSPCs that confer a selective advantage and allow for clonal cell expansion.•This clonal population of mutated HSPCs can give rise to leukocytes with altered immune properties, and this condition can adversely impact the cardiovascular system.•Clonal hematopoiesis may represent a new causal risk factor for cardiovascular disease that can add to the predictive value of the traditional risk factors.•Understanding the clonal hematopoiesis status of a patient could aid in the development of personalized strategies for anti-inflammatory therapies for cardiovascular disease. Heart failure is a common disease with poor prognosis that is associated with cardiac immune cell infiltration and dysregulated cytokine expression. Recently, the clonal expansion of hematopoietic cells with acquired (i.e., nonheritable) DNA mutations, a process referred to as clonal hematopoiesis, has been reported to be associated with cardiovascular diseases including heart failure. Mechanistic studies have shown that leukocytes that harbor these somatic mutations display altered inflammatory characteristics that worsen the phenotypes associated with heart failure in experimental models. In this review, we summarize recent epidemiological and experimental evidence that support the hypothesis that clonal hematopoiesis-mediated immune cell dysfunction contributes to heart failure and cardiovascular disease in general. [Display omitted]
ISSN:2452-302X
2452-302X
DOI:10.1016/j.jacbts.2019.08.006