Evidence map›Paper›PMID 33955206›Full record

ArticleESC heart failure2021

Ubiquitin-proteasome-system and enzymes of energy metabolism in skeletal muscle of patients with HFpEF and HFrEF.

Volker Adams, Sebastian Wunderlich, Norman Mangner, Jennifer Hommel, Katrin Esefeld, Stephan Gielen, Martin Halle, Øyvind Ellingsen, Emeline M Van Craenenbroeck, Ulrik Wisløff and 3 more

Open access · goldAbstract read
In one paragraph

Article in ESC heart failure, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 9% of its field
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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

19 citing papers in PubMed, 24 citations in OpenAlex.

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  13. Locomotor and respiratory muscle abnormalities in HFrEF and HFpEF.Frontiers in cardiovascular medicine · 2023
    Review
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  15. Empagliflozin Preserves Skeletal Muscle Function in a HFpEF Rat Model.International journal of molecular sciences · 2022
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4 · The record

Corrections and comments

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

13 authors at 7 institutions in 3 countries.

Volker AdamsDepartment of Internal Medicine and Cardiology, Technische Universität Dresden, Heart Center Dresden - University Hospital, Herzzentrum Dresden, Universitätsklinik, Fetscherstraße 76, Dresden, 01307, Germany.
Sebastian WunderlichDepartment of Internal Medicine/Cardiology, Heart Center Leipzig - University Hospital, Leipzig, Germany.
Norman MangnerDepartment of Internal Medicine and Cardiology, Technische Universität Dresden, Heart Center Dresden - University Hospital, Herzzentrum Dresden, Universitätsklinik, Fetscherstraße 76, Dresden, 01307, Germany.
Jennifer HommelDepartment of Internal Medicine and Cardiology, Technische Universität Dresden, Heart Center Dresden - University Hospital, Herzzentrum Dresden, Universitätsklinik, Fetscherstraße 76, Dresden, 01307, Germany.
Katrin EsefeldDZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany.
Stephan GielenDepartment of Cardiology, Angiology and Intensive Care, Klinikum Lippe, Detmold, Germany.
Martin HalleDZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany.
Øyvind EllingsenDepartment of Cardiology, St. Olavs University Hospital, Trondheim, Norway.
Emeline M Van CraenenbroeckDepartment of Cardiology, Antwerp University Hospital, Edegem, Belgium.
Ulrik WisløffThe Cardiac Exercise Research Group at Department of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway.
Burkert PieskeDepartment Internal Medicine and Cardiology, Campus Virchow Klinikum, Charité Universitätsmedizin Berlin, Berlin, Germany.
Axel LinkeDepartment of Internal Medicine and Cardiology, Technische Universität Dresden, Heart Center Dresden - University Hospital, Herzzentrum Dresden, Universitätsklinik, Fetscherstraße 76, Dresden, 01307, Germany.
Ephraim B WinzerDepartment of Internal Medicine and Cardiology, Technische Universität Dresden, Heart Center Dresden - University Hospital, Herzzentrum Dresden, Universitätsklinik, Fetscherstraße 76, Dresden, 01307, Germany.ORCID 0000-0002-1752-8528
Klinik und Poliklinik für Psychotherapie und Psychosomatik · DENorwegian University of Science and Technology · NOTUM Klinikum · DECharité - Universitätsmedizin Berlin · DEKlinikum Lippe · DELeipzig Heart Institute · DEUniversity of Antwerp · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSkeletal muscle (SM) alterations contribute to exercise intolerance in heart failure patients with preserved (HFpEF) or reduced (HFrEF) left ventricular ejection fraction (LVEF). Protein degradation via the ubiquitin-proteasome-system (UPS), nuclear apoptosis, and reduced mitochondrial energy supply is associated with SM weakness in HFrEF. These mechanisms are incompletely studied in HFpEF, and a direct comparison between these groups is missing. METHODS AND

resultsPatients with HFpEF (LVEF ≥ 50%, septal E/e' > 15 or >8 and NT-proBNP > 220 pg/mL, n = 20), HFrEF (LVEF ≤ 35%, n = 20) and sedentary control subjects (Con, n = 12) were studied. Inflammatory markers were measured in serum, and markers of the UPS, nuclear apoptosis, and energy metabolism were determined in percutaneous SM biopsies. Both HFpEF and HFrEF showed increased proteolysis (MuRF-1 protein expression, ubiquitination, and proteasome activity) with proteasome activity significantly related to interleukin-6. Proteolysis was more pronounced in patients with lower exercise capacity as indicated by peak oxygen uptake in per cent predicted below the median. Markers of apoptosis did not differ between groups. Mitochondrial energy supply was reduced in HFpEF and HFrEF (complex-I activity: -31% and -53%; malate dehydrogenase activity: -20% and -29%; both P < 0.05 vs. Con). In contrast, short-term energy supply via creatine kinase was increased in HFpEF but decreased in HFrEF (47% and -45%; P < 0.05 vs. Con).

conclusionsSimilarly to HFrEF, skeletal muscle in HFpEF is characterized by increased proteolysis linked to systemic inflammation and reduced exercise capacity. Energy metabolism is disturbed in both groups; however, its regulation seems to be severity-dependent.

Indexed as

Heart FailureEnergy MetabolismHumansMuscle, SkeletalProteasome Endopeptidase ComplexStroke VolumeUbiquitinVentricular Function, LeftProteasome Endopeptidase ComplexUbiquitinAtrophyDiastolic heart failureHeart failureMitochondriaSkeletal muscle exerciseUbiquitin-proteasome system genetics

Identifiers

PMID33955206
PMCPMC8318515
OpenAlexW3158626794

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.