Evidence map›Paper›PMID 42192415›Full record

ArticleCardiovascular diabetology2026

Exerkine dysregulation links visceral adiposity to skeletal muscle impairment in end-stage heart failure with reduced ejection fraction: proteomic evidence for a cardio-adipose-muscle axis.

Marta Załęska-Kocięcka, Maciej Mazuruk, Karolina Szcześniak, Piotr Łaba, Marta Kacperska, Łukasz Nogajski, Maksymilian Nowakowski, Maciej Mączewski, Hanna Czerwińska, Miłosz Rosa and 10 more

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Article in Cardiovascular diabetology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors.

Marta Załęska-Kocięcka *Heart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland. mzaleska@ikard.pl.
Maciej Mazuruk *Heart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.
Karolina SzcześniakHeart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.
Piotr ŁabaHeart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.
Marta KacperskaHeart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.
Łukasz NogajskiHeart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.
Maksymilian NowakowskiHeart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.
Maciej MączewskiHeart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.
Hanna CzerwińskaHeart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.
Miłosz RosaHeart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.
Piotr OlbryśHeart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.
Aleksandra MączyńskaDepartment of Clinical Physiology, Centre of Postgraduate Medical Education, Warsaw, Poland.
Jarosław KuriataDepartment of Cardiac Surgery, National Institute of Cardiology, Warsaw, Poland.
Piotr KołsutDepartment of Cardiac Surgery, National Institute of Cardiology, Warsaw, Poland.
Zuzanna WojdyńskaHeart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.
Ilona MichałowskaDepartment of Radiology, National Institute of Cardiology, Warsaw, Poland.
Aleksandra PaterekHeart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.
Przemysław BłyszczukHeart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.
Przemysław Leszek *Heart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.
Michał Mączewski *Heart Failure and Transplantology Department, Mechanical Circulatory Support and Transplant Department, National Institute of Cardiology, Warsaw, Poland.

Funding

Agency for Medical Research (ABM) KPOD.07.07-IW.07-0149/24National Institute of Cardiology, Warsaw statutory grant 2.20/VII/23National Institute of Cardiology, Warsaw, Poland statutory grant 1.2.17/VII/23National Science Centre (NCN) 2024/55/D/NZ4/01538
6 · The paper itself

Abstract

backgroundHeart failure with reduced ejection fraction (HFrEF) is associated with profound alterations in body composition, skeletal muscle dysfunction, and impaired exercise capacity. Exerkines representing exercise-responsive signaling molecules released by skeletal muscle, adipose tissue, and other organs may mediate systemic metabolic communication between tissues. However, their role in advanced HFrEF and their relationship with adiposity and skeletal muscle characteristics remain poorly understood.

methodsWe studied 73 patients with end-stage HFrEF and 16 healthy controls. Body composition was assessed using computed tomography, including visceral (VAT), subcutaneous (SAT), and epicardial adipose tissue (EAT), as well as skeletal muscle quantity (psoas muscle index, PMI) and quality (psoas muscle density, PMD). Functional performance was evaluated using handgrip strength (HGT) and the 6-min walk test (6MWT). Circulating exerkines were quantified using the Olink technology. Associations between proteins and clinical variables were assessed using age- and creatinine-adjusted linear models with false discovery rate correction.

resultsAmong patients with HFrEF, 36% were obese and 38% exhibited central obesity independent of BMI. Muscle strength and muscle quality were strongly associated with functional capacity. VAT correlated with muscle mass but not with muscle quality or performance. Compared with controls, HFrEF patients demonstrated elevated inflammatory and metabolic stress-related exerkines including CXCL8, CCL2, IL-6, TNF, IL-15, GDF15, FGF21, ANGPTL4, CTSB, DCN, and resistin. In contrast, proteins associated with muscle integrity and regenerative signaling (myostatin, BDNF, IL-7, SPARC) were significantly reduced. In HFrEF patients leptin strongly correlated with adiposity measures. Metabolic stress mediators (GDF15, IL-15, FGF21, CTSB) were inversely associated with muscle quality and functional performance, whereas myostatin positively correlated with muscle quality, strength, and exercise capacity. BDNF was inversely associated with frailty.

conclusionsAdvanced HFrEF is characterized by a dysregulated exerkine network linking adiposity, skeletal muscle quality, and functional performance. Four biologically coherent axes were identified: a leptin-driven adiposity axis, a metabolic stress-muscle quality axis, a myostatin-related muscle function axis, and a neurotrophic frailty axis. These findings support the presence of a systemic cardio-adipose-muscle signaling network in end-stage HFrEF and identify candidate molecular mediators of sarcopenia and functional decline.

Indexed as

AdipokinesAdiposityHeart FailureIntra-Abdominal FatMuscle, SkeletalObesity, AbdominalProteomicsStroke VolumeVentricular Function, LeftAgedBiomarkersCase-Control StudiesEpicardial Adipose TissueExercise ToleranceFemaleHand StrengthAdipokinesBiomarkersMyokinesAdipose tissueExerkinesHeart failure with reduced ejection fractionInflammationObesitySarcopeniaSkeletal muscles

Identifiers

PMID42192415
PMCPMC13393631

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.