Clonal Hematopoiesis of Indeterminate Potential and Atrial Fibrillation: Insights into Pathophysiology and Clinical Implications DOI Open Access
Paschalis Karakasis, Panagiotis Theofilis, Eleftheria Lefkou

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(6), P. 2739 - 2739

Published: March 18, 2025

Clonal hematopoiesis of indeterminate potential (CHIP) has emerged as a novel risk factor for cardiovascular diseases. CHIP is characterized by the expansion hematopoietic stem cell clones harboring somatic mutations in genes such TET2, DNMT3A, and ASXL1, which are implicated inflammation, atrial remodeling, hypercoagulability. These foster pro-inflammatory pro-thrombotic environment conducive to arrhythmogenesis, thereby linking development progression fibrillation (AF). Mechanistic insights indicate that contributes fibrosis, disrupts calcium signaling, exacerbates oxidative stress, all heighten susceptibility AF. Clinical studies, including epidemiological Mendelian randomization analyses, further support association between an increased both incident progressive AF, with specific TET2 ASXL1 identified significant contributors. Additionally, been linked adverse outcomes elevated rates heart failure, thromboembolism, mortality. Understanding CHIP’s role AF pathophysiology offers opportunities precision medicine approaches, providing avenues early intervention targeted treatment. This review synthesizes current mechanistic clinical evidence on emphasizes its biomarker stratification, explores emerging therapeutic strategies targeting CHIP-associated pathways.

Language: Английский

Clonal Hematopoiesis of Indeterminate Potential and Atrial Fibrillation: Insights into Pathophysiology and Clinical Implications DOI Open Access
Paschalis Karakasis, Panagiotis Theofilis, Eleftheria Lefkou

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(6), P. 2739 - 2739

Published: March 18, 2025

Clonal hematopoiesis of indeterminate potential (CHIP) has emerged as a novel risk factor for cardiovascular diseases. CHIP is characterized by the expansion hematopoietic stem cell clones harboring somatic mutations in genes such TET2, DNMT3A, and ASXL1, which are implicated inflammation, atrial remodeling, hypercoagulability. These foster pro-inflammatory pro-thrombotic environment conducive to arrhythmogenesis, thereby linking development progression fibrillation (AF). Mechanistic insights indicate that contributes fibrosis, disrupts calcium signaling, exacerbates oxidative stress, all heighten susceptibility AF. Clinical studies, including epidemiological Mendelian randomization analyses, further support association between an increased both incident progressive AF, with specific TET2 ASXL1 identified significant contributors. Additionally, been linked adverse outcomes elevated rates heart failure, thromboembolism, mortality. Understanding CHIP’s role AF pathophysiology offers opportunities precision medicine approaches, providing avenues early intervention targeted treatment. This review synthesizes current mechanistic clinical evidence on emphasizes its biomarker stratification, explores emerging therapeutic strategies targeting CHIP-associated pathways.

Language: Английский

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