Evidence map›Paper›PMID 36475881›Full record

ArticleThe American journal of sports medicine2023

Depressed Protein Synthesis and Anabolic Signaling Potentiate ACL Tear-Resultant Quadriceps Atrophy.

Alexander R Keeble, Camille R Brightwell, Christine M Latham, Nicholas T Thomas, C Brooks Mobley, Kevin A Murach, Darren L Johnson, Brian Noehren, Christopher S Fry

Open access · greenAbstract read
In one paragraph

Article in The American journal of sports medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Article
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  5. Article
  6. Muscle atrophy after ACL reconstruction involves molecular mechanisms beyond unloading.Journal of applied physiology (Bethesda, Md. : 1985) · 2026
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  15. Blood Flow Restriction Training in the Young Athlete.HSS journal : the musculoskeletal journal of Hospital for Special Surgery · 2024
    Article
  16. Article
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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

9 authors at 1 institution in 1 country.

Alexander R KeebleDepartment of Physiology, College of Medicine, University of Kentucky, Lexington, Kentucky, USA.
Camille R BrightwellCenter for Muscle Biology, University of Kentucky, Lexington, Kentucky, USA.
Christine M LathamCenter for Muscle Biology, University of Kentucky, Lexington, Kentucky, USA.
Nicholas T ThomasCenter for Muscle Biology, University of Kentucky, Lexington, Kentucky, USA.
C Brooks MobleyDepartment of Physiology, College of Medicine, University of Kentucky, Lexington, Kentucky, USA.
Kevin A MurachCenter for Muscle Biology, University of Kentucky, Lexington, Kentucky, USA.
Darren L JohnsonDepartment of Orthopaedic Surgery and Sports Medicine, University of Kentucky, Lexington, Kentucky, USA.
Brian NoehrenCenter for Muscle Biology, University of Kentucky, Lexington, Kentucky, USA.
Christopher S FryCenter for Muscle Biology, University of Kentucky, Lexington, Kentucky, USA.ORCID 0000-0002-4207-6594
University of Kentucky · US

Funding

Myostatin Alters Muscle Composition as The Result of an ACL InjuryR01AR072061 · NIAMS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI FRY, CHRISTOPHER · 2018 to 2023
$2.2M
NIAMS NIH HHS R01 AR072061
6 · The paper itself

Abstract

backgroundAnterior cruciate ligament (ACL) tear (ACLT) leads to protracted quadriceps muscle atrophy. Protein turnover largely dictates muscle size and is highly responsive to injury and loading. Regulation of quadriceps molecular protein synthetic machinery after ACLT has largely been unexplored, limiting development of targeted therapies. PURPOSE: To define the effect of ACLT on (1) the activation of protein synthetic and catabolic signaling within quadriceps biopsy specimens from human participants and (2) the time course of alterations to protein synthesis and its molecular regulation in a mouse ACL injury model. STUDY

designDescriptive laboratory study.

methodsMuscle biopsy specimens were obtained from the ACL-injured and noninjured vastus lateralis of young adult humans after an overnight fast (N = 21; mean ± SD, 19 ± 5 years). Mice had their limbs assigned to ACLT or control, and whole quadriceps were collected 6 hours or 1, 3, or 7 days after injury with puromycin injected before tissue collection for assessment of relative protein synthesis. Muscle fiber size and expression and phosphorylation of protein anabolic and catabolic signaling proteins were assessed at the protein and transcript levels (RNA sequencing).

resultsHuman quadriceps showed reduced phosphorylation of ribosomal protein S6 (-41%) in the ACL-injured limb (

conclusion(1) Global protein synthesis and anabolic signaling deficits occur in the quadriceps in response to ACL injury, without notable changes in measured markers of muscle protein catabolism. (2) Importantly, these deficits occur before the onset of significant atrophy, underscoring the need for early intervention. CLINICAL RELEVANCE: These findings suggest that blunted protein anabolism as opposed to increased catabolism likely mediates quadriceps atrophy after ACL injury. Thus, future interventions should aim to restore muscle protein anabolism rapidly after ACLT.

Indexed as

Anterior Cruciate Ligament InjuriesAnimalsHumansMiceMuscle Fibers, SkeletalMuscle ProteinsMuscular AtrophyQuadriceps MuscleYoung AdultMuscle Proteinsanterior cruciate ligamentE3 ubiquitin ligaseprotein metabolismskeletal muscle

Identifiers

PMID36475881
PMCPMC9813974
OpenAlexW4310945991

What OpenQuestion holds

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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.