Exploring the MicroRNA Landscape in Cardiac Amyloidosis: Molecular Insights and Clinical Applications

Исследование профиля микроРНК при кардиальном амилоидозе: молекулярные аспекты и клиническое применение
Joanna Kontaraki, Anthoula Plevritaki, Aleksi Sallo, Konstantinos Fragkiadakis, E. M. Kallergis, Evangelos Zacharis, John Kopidakis, Emmanouil Kampanieris, Sophia Achladianaki, Vasiliki Papakosta, Emmanouil Simantirakis, Maria Marketou
2026-03-23

RNA-based therapeuticscardiac amyloidosislight-chain amyloidosismicroRNA profilingtransthyretin amyloidosis
BACKGROUND: Cardiac amyloidosis (CA) is an increasingly recognized cause of heart failure with preserved ejection fraction, resulting from myocardial deposition of misfolded amyloid fibrils derived predominantly from transthyretin (ATTR wild-type [ATTRwt] or variant [ATTRv]) or immunoglobulin light chains (AL). Despite advances in noninvasive imaging and disease-modifying therapies, delayed diagnosis remains common, and clinically actionable molecular biomarkers for early detection, phenotypic discrimination, and therapeutic monitoring are limited. MicroRNAs (miRNAs), small noncoding regulators of post-transcriptional gene expression, have emerged as key modulators of cardiovascular remodeling and systemic amyloid biology. METHODS: We performed a comprehensive review of experimental, translational, and clinical studies to evaluate the role of miRNAs in transthyretin and light-chain cardiac amyloidosis, incorporating data from myocardial tissue analyses, circulating miRNA profiling, and mechanistic studies in cellular and animal models. RESULTS: Dysregulated miRNA networks contribute to amyloid-induced cardiac injury by modulating mitochondrial energetics, oxidative stress, inflammation, fibrosis, proteostasis, and neurocardiac signaling. Specific miRNAs, including members of the miR-21, miR-29, and miR-30 families, as well as miR-150-5p and miR-339, have been associated with amyloid burden, adverse myocardial remodeling, plasma cell biology, and disease severity. Distinct circulating and tissue miRNA signatures differentiate transthyretin from light-chain cardiac amyloidosis and correlate with functional status, heart failure biomarkers, and clinical outcomes. CONCLUSIONS: MiRNAs represent promising diagnostic and prognostic biomarkers in cardiac amyloidosis and offer mechanistic insights into disease pathogenesis. Integration of miRNA profiling with multimodality imaging and emerging RNA-based therapeutics may enable earlier diagnosis and support precision management of amyloid-related heart failure.
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Circulating and tissue microRNA signatures can differentiate transthyretin from light-chain cardiac amyloidosis.
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Combining microRNA profiling with multimodality imaging and RNA-based therapeutics may enable earlier diagnosis and more precise cardiac amyloidosis management.
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Dysregulated microRNA networks contribute to cardiac amyloidosis injury through effects on mitochondrial energetics, oxidative stress, inflammation, fibrosis, proteostasis, and neurocardiac signaling.
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MicroRNA profiles correlate with functional status, heart-failure biomarkers, and clinical outcomes, supporting diagnostic and prognostic applications.
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miR-21, miR-29, miR-30 family members, miR-150-5p, and miR-339 are associated with amyloid burden, myocardial remodeling, plasma cell biology, and disease severity.

cardiac amyloidosis, including transthyretin and light-chain cardiac amyloidosis

the roles, dysregulation, and biomarker potential of microRNAs in amyloid-induced cardiac injury, disease discrimination, severity assessment, and therapeutic monitoring

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2026-03-23
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Joanna Kontaraki
Anthoula Plevritaki
Aleksi Sallo
Konstantinos Fragkiadakis
E. M. Kallergis
Evangelos Zacharis
John Kopidakis
Emmanouil Kampanieris
Sophia Achladianaki
Vasiliki Papakosta
Emmanouil Simantirakis
Maria Marketou
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