Evidence map›Paper›PMID 39434377›Full record

ReviewMedical science monitor : international medical journal of experimental and clinical research2024

Targeting MuRF1 to Combat Skeletal Muscle Wasting in Cardiac Cachexia: Mechanisms and Therapeutic Prospects.

Xiaotong Liu, Ya Wen, Yanmei Lu

Abstract readReview
In one paragraph

Review in Medical science monitor : international medical journal of experimental and clinical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Article
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

3 authors.

Xiaotong LiuDepartment of Cardiac Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.
Ya WenDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Yanmei LuDepartment of Cardiac Pacing and Electrophysiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China.ORCID 0000-0002-7293-8634

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac cachexia, the terminal stage of chronic heart failure, is characterized by severe systemic metabolic imbalances and significant weight loss, primarily resulting from skeletal muscle mass depletion. Despite the detrimental consequences, there is no standardized and clinically-approved intervention currently available for cardiac cachexia. In the context of cardiac cachexia, accelerated protein turnover, that is, inhibited protein synthesis and enhanced protein degradation, plays a crucial role in skeletal muscle wasting. This process is primarily mediated by various proteins encoded by atrogenes. Among them, the atrogene Trim63 (tripartite motif family 63) and its encoded protein MuRF1 have been extensively studied. This review article aims to elucidate the pathogenic mechanisms underlying skeletal muscle wasting in cardiac cachexia, describe the biochemical characteristics of MuRF1, and provide an overview of the investigation into MuRF1-targeting inhibitors. The ultimate goal is to offer novel strategies for the clinical treatment for skeletal muscle wasting associated with cardiac cachexia.

Indexed as

CachexiaHeart FailureMuscle ProteinsMuscle, SkeletalMuscular AtrophyTripartite Motif ProteinsUbiquitin-Protein LigasesAnimalsHumansMuscle ProteinsTRIM63 protein, humanTripartite Motif ProteinsUbiquitin-Protein Ligases

Identifiers

PMID39434377
PMCPMC11512513

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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 OpenQuestion graph.