Evidence map›Paper›PMID 32858949›Full record

ReviewCells2020

Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and Atrophy.

Tadashi Yoshida, Patrice Delafontaine

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 431 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
431citing papers in PubMed, 5 pooled it
20.5field-weighted citation impact, top 1% 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

431 citing papers in PubMed, 5 syntheses or guidelines pooled it, 635 citations in OpenAlex.

  1. Circulating biomarkers in older adults with and without sarcopenia: a systematic review and meta-analysis.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026
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371 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Tadashi YoshidaHeart and Vascular Institute, John W. Deming Department of Medicine, Tulane University School of Medicine, 1430 Tulane Ave SL-48, New Orleans, LA 70112, USA.ORCID 0000-0002-4544-1497
Patrice DelafontaineHeart and Vascular Institute, John W. Deming Department of Medicine, Tulane University School of Medicine, 1430 Tulane Ave SL-48, New Orleans, LA 70112, USA.
Tulane University · US

Funding

Tracking & Evaluation CoreU54GM104940 · NIGMS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI Peter Todd Katzmarzyk · 2012 to 2026
$69.1M
Insulin-Like Growth Factor-1and AtherosclerosisR01HL070241 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI PATRICE DELAFONTAINE · 2003 to 2026
$10.1M
Translational Research in Hypertension and Renal BiologyP30GM103337 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI NAVAR, LUIS GABRIEL · 2012 to 2016
$5.8M
ANGIOTENSIN II, IGF-1 AND SKELETAL MUSCLE ATROPHYR01HL080682 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI DELAFONTAINE, PATRICE · 2007 to 2015
$3.3M
NHLBI NIH HHS R01 HL070241NHLBI NIH HHS R01 HL080682NIGMS NIH HHS P30 GM103337NIGMS NIH HHS U54 GM104940
6 · The paper itself

Abstract

Insulin-like growth factor-1 (IGF-1) is a key growth factor that regulates both anabolic and catabolic pathways in skeletal muscle. IGF-1 increases skeletal muscle protein synthesis via PI3K/Akt/mTOR and PI3K/Akt/GSK3β pathways. PI3K/Akt can also inhibit FoxOs and suppress transcription of E3 ubiquitin ligases that regulate ubiquitin proteasome system (UPS)-mediated protein degradation. Autophagy is likely inhibited by IGF-1 via mTOR and FoxO signaling, although the contribution of autophagy regulation in IGF-1-mediated inhibition of skeletal muscle atrophy remains to be determined. Evidence has suggested that IGF-1/Akt can inhibit muscle atrophy-inducing cytokine and myostatin signaling via inhibition of the NF-κΒ and Smad pathways, respectively. Several miRNAs have been found to regulate IGF-1 signaling in skeletal muscle, and these miRs are likely regulated in different pathological conditions and contribute to the development of muscle atrophy. IGF-1 also potentiates skeletal muscle regeneration via activation of skeletal muscle stem (satellite) cells, which may contribute to muscle hypertrophy and/or inhibit atrophy. Importantly, IGF-1 levels and IGF-1R downstream signaling are suppressed in many chronic disease conditions and likely result in muscle atrophy via the combined effects of altered protein synthesis, UPS activity, autophagy, and muscle regeneration.

Indexed as

HumansHypertrophyInsulin-Like Growth Factor IMuscle, SkeletalMuscular AtrophySignal TransductionInsulin-Like Growth Factor Iatrophyautophagycachexiahypertrophyinsulin-like growth factor-1muscle regenerationskeletal muscle

Identifiers

PMID32858949
PMCPMC7564605
OpenAlexW3080836913

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.