Integrated miRNA-cytokine profiling reveals a molecular signature of cachexia in patients with chronic heart failure.
4 affiliations
- 1Department of Translational and Precision Medicine, Sapienza University of Rome, Viale dell'Università 37, 00185 Rome, Italy.
- 2Experimental Immunology Laboratory, Istituto Dermopatico dell'Immacolata (IDI-IRCCS), Rome, Italy.
- 3Department of Cardiology (CVK) of German Heart Center Charité, German Centre for Cardiovascular Research (DZHK) Partner Site Berlin, Charité Universitätsmedizin, Berlin, Germany.
- 4Department of Interdisciplinary Studies on WellBeing, Health and Environmental Sustainability (BeSSA), Sapienza University of Rome, Rieti, Italy.
Abstract
Introduction
Cardiac cachexia (CC) complicates chronic heart failure (CHF). Circulating microRNAs (miRNAs) and cytokines, such as growth differentiation factor-15 (GDF-15) and fibroblast growth factor-21 (FGF-21), may reflect the catabolic-anabolic imbalance and structural remodelling associated with this syndrome. To define the circulating signature of CHF by profiling muscle and remodelling-related miRNAs alongside GDF-15 and FGF-21, and to assess their associations with cardiac function and clinical phenotypes.Methods
Twenty-five CHF patients (median age 78.0 years, 40% male) and 10 controls (median age 56.8 years, 60% male) were studied. CC was defined as unintentional, non-oedematous weight loss ≥6% within 6 months. Circulating miRNAs were quantified by RT-qPCR, GDF-15 and FGF-21 by ELISA. CHF patients were classified as having reduced (HFrEF) or preserved ejection fraction (HFpEF). Associations with CC and clinical CHF phenotypes were evaluated.Results
Compared with controls, CHF patients showed lower levels of miR-15b, miR-29b, miR-133a, and miR-486 (all P < .01) and elevated GDF-15 levels (P < .001). FGF-21 was higher in patients with CC (P = .012), in HFrEF vs HFpEF (P = .039), and in NYHA III-IV vs I-II (P = .05). miR-29b levels were lower in CC (P = .019) and in HFrEF + CC vs HFpEF + nCC (P = .019). In CC, FGF-21 inversely correlated with miR-486 (ρ = -.69, P = .035), whereas GDF-15 inversely correlated with miR-21 (ρ = -.81, P = .007).Conclusions
CHF is associated with miRNA suppression and elevated stress cytokine levels, amplified in CC. miR-29b and FGF-21 showed associations with CC, functional impairment, and structural remodelling, warranting validation in larger longitudinal cohorts.
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BibTeX
@article{tambaro2026integrated,
title = {{Integrated miRNA-cytokine profiling reveals a molecular signature of cachexia in patients with chronic heart failure.}},
author = {Federica Tambaro and Giovanni Imbimbo and Carmen Gallicchio and Paolo Nardozi and Simona Orlando and Roberta Belli and Cesarina Ramaccini and Stefan D Anker and Alessio Molfino and Maurizio Muscaritoli},
journal = {ESC heart failure},
year = {2026},
month = aug,
doi = {10.1093/eschf/xvag229},
url = {https://europepmc.org/article/MED/42853063},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - Integrated miRNA-cytokine profiling reveals a molecular signature of cachexia in patients with chronic heart failure.
AU - Federica Tambaro
AU - Giovanni Imbimbo
AU - Carmen Gallicchio
AU - Paolo Nardozi
AU - Simona Orlando
AU - Roberta Belli
AU - Cesarina Ramaccini
AU - Stefan D Anker
AU - Alessio Molfino
AU - Maurizio Muscaritoli
PY - 2026
DA - 2026/08/01
JO - ESC heart failure
DO - 10.1093/eschf/xvag229
UR - https://europepmc.org/article/MED/42853063
AB - Introduction Cardiac cachexia (CC) complicates chronic heart failure (CHF). Circulating microRNAs (miRNAs) and cytokines, such as growth differentiation factor-15 (GDF-15) and fibroblast growth factor-21 (FGF-21), may reflect the catabolic-anabolic imbalance and structural remodelling associated with this syndrome. To define the circulating signature of CHF by profiling muscle and remodelling-related miRNAs alongside GDF-15 and FGF-21, and to assess their associations with cardiac function and clinical phenotypes.Methods Twenty-five CHF patients (median age 78.0 years, 40% male) and 10 controls (median age 56.8 years, 60% male) were studied. CC was defined as unintentional, non-oedematous weight loss ≥6% within 6 months. Circulating miRNAs were quantified by RT-qPCR, GDF-15 and FGF-21 by ELISA. CHF patients were classified as having reduced (HFrEF) or preserved ejection fraction (HFpEF). Associations with CC and clinical CHF phenotypes were evaluated.Results Compared with controls, CHF patients showed lower levels of miR-15b, miR-29b, miR-133a, and miR-486 (all P < .01) and elevated GDF-15 levels (P < .001). FGF-21 was higher in patients with CC (P = .012), in HFrEF vs HFpEF (P = .039), and in NYHA III-IV vs I-II (P = .05). miR-29b levels were lower in CC (P = .019) and in HFrEF + CC vs HFpEF + nCC (P = .019). In CC, FGF-21 inversely correlated with miR-486 (ρ = -.69, P = .035), whereas GDF-15 inversely correlated with miR-21 (ρ = -.81, P = .007).Conclusions CHF is associated with miRNA suppression and elevated stress cytokine levels, amplified in CC. miR-29b and FGF-21 showed associations with CC, functional impairment, and structural remodelling, warranting validation in larger longitudinal cohorts.
SN - 2055-5822
ER -