Evidence map›Paper›PMID 33225593›Full record

ReviewESC heart failure2021

Skeletal muscle atrophy in heart failure with diabetes: from molecular mechanisms to clinical evidence.

Nathanael Wood, Sam Straw, Mattia Scalabrin, Lee D Roberts, Klaus K Witte, Thomas Scott Bowen

Open access · goldAbstract readReview
In one paragraph

Review 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
1.2field-weighted citation impact, top 22% 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, 31 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Observational
  13. Article
  14. Review
  15. Biophysics reviews · 2022
    Review
  16. Article
  17. Review
  18. Article
  19. Review
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

6 authors at 1 institution in 1 country.

Nathanael WoodFaculty of Biomedical Sciences, University of Leeds, Leeds, LS2 9JT, UK.
Sam StrawLeeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, UK.
Mattia ScalabrinFaculty of Biomedical Sciences, University of Leeds, Leeds, LS2 9JT, UK.
Lee D RobertsLeeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, UK.
Klaus K WitteLeeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, UK.
Thomas Scott BowenFaculty of Biomedical Sciences, University of Leeds, Leeds, LS2 9JT, UK.
University of Leeds · GB

Funding

British Heart Foundation FS/CRTF/20/24071British Heart Foundation PG/19/3/34133Medical Research Council MR/S025472/1
6 · The paper itself

Abstract

Two highly prevalent and growing global diseases impacted by skeletal muscle atrophy are chronic heart failure (HF) and type 2 diabetes mellitus (DM). The presence of either condition increases the likelihood of developing the other, with recent studies revealing a large and relatively poorly characterized clinical population of patients with coexistent HF and DM (HFDM). HFDM results in worse symptoms and poorer clinical outcomes compared with DM or HF alone, and cardiovascular-focused disease-modifying agents have proven less effective in HFDM indicating a key role of the periphery. This review combines current clinical knowledge and basic biological mechanisms to address the critical emergence of skeletal muscle atrophy in patients with HFDM as a key driver of symptoms. We discuss how the degree of skeletal muscle wasting in patients with HFDM is likely underpinned by a variety of mechanisms that include mitochondrial dysfunction, insulin resistance, inflammation, and lipotoxicity. Given many atrophic triggers (e.g. ubiquitin proteasome/autophagy/calpain activity and supressed IGF1-Akt-mTORC1 signalling) are linked to increased production of reactive oxygen species, we speculate that a higher pro-oxidative state in HFDM could be a unifying mechanism that promotes accelerated fibre atrophy. Overall, our proposal is that patients with HFDM represent a unique clinical population, prompting a review of treatment strategies including further focus on elucidating potential mechanisms and therapeutic targets of muscle atrophy in these distinct patients.

Indexed as

Diabetes Mellitus, Type 2Heart FailureHumansMuscle, SkeletalMuscular AtrophySignal TransductionAnabolicDMHFrEFInsulinMuscle wastingProteolysis

Identifiers

PMID33225593
PMCPMC7835554
OpenAlexW3106587771

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.