Evidence map›Paper›PMID 36738276›Full record

ReviewThe journals of gerontology. Series A, Biological sciences and medical sciences2023

Challenges and Future Prospects of Targeting Myostatin/Activin A Signaling to Treat Diseases of Muscle Loss and Metabolic Dysfunction.

Se-Jin Lee, Shalender Bhasin, Lloyd Klickstein, Venkatesh Krishnan, Daniel Rooks

Open access · bronzeAbstract readReview
In one paragraph

Review in The journals of gerontology. Series A, Biological sciences and medical sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 36 citations in OpenAlex.

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  15. Rethinking Osteoporosis Drugs: Can We Simultaneously Address Sarcopenia?International journal of molecular sciences · 2025
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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

5 authors at 4 institutions in 1 country.

Se-Jin LeeThe Jackson Laboratory for Genomic Medicine, Farmington, Connecticut, USA.
Shalender BhasinResearch Program in Men's Health: Aging and Metabolism, Boston Claude D. Pepper Older Americans Independence Center, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.ORCID 0000-0002-3982-6200
Lloyd KlicksteinVersanis Bio, Inc., Oakland, California, USA.
Venkatesh KrishnanEli Lilly, Inc., Indianapolis, Indiana, USA.
Daniel RooksTranslational Medicine, Novartis Institute for BioMedical Research, Inc., Cambridge, Massachusetts, USA.
Brigham and Women's Hospital · USEli Lilly (United States) · USNovartis (United States) · USUniversity of Connecticut · US

Funding

TUFTS--FIELDINGP30AG031679 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI Ravi Jasuja · 2008 to 2026
$23.9M
Characterization of Myostatin and GDF-11R01AR060636 · NIAMS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI LEE, SE-JIN · 2010 to 2020
$3.7M
Extracellular regulation of bone mass by transforming growth factor-ß-related ligands and their binding proteinsR01AR081659 · NIAMS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI EMILY L GERMAIN-LEE, Se-Jin Lee · 2022 to 2026
$3.1M
Regulation of GDF11 by extracellular mechanismsR01AG072087 · NIA · UNIVERSITY OF CINCINNATI · PI THOMPSON, THOMAS B · 2020 to 2024
$2.8M
TGF-beta family members and their binding proteins in aging skeletal muscleR01AG052962 · NIA · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI LEE, SE-JIN, RANDO, THOMAS A. · 2017 to 2020
$1.9M
TESTOSTERONE REPLACEMENT &PHYSICAL FUNCTION IN HIV+MENR01DK049296 · NIDDK · LA BIOMED RES INST/ HARBOR UCLA MED CTR · PI BHASIN, SHALENDAR · 1994 to 2005
$1.7M
Anti-Geronic Factors, GDF11 and Oxytocin, and Aging-Related PhenotypesR56AG052972 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI BHASIN, SHALENDER · 2016 to 2017
$353k
NIAMS NIH HHS R01 AR060636NIAMS NIH HHS R01 AR081659NIA NIH HHS P30 AG031679NIA NIH HHS R01 AG052962NIA NIH HHS R01 AG072087NIA NIH HHS R56 AG052972NIDDK NIH HHS R01 DK049296NIH HHS R01AG052962
6 · The paper itself

Abstract

Over the past 25 years, considerable progress has been made in terms of elucidating the regulatory and signaling mechanisms underlying the control of skeletal muscle mass by myostatin and other secreted proteins belonging to the transforming growth factor-β superfamily. Preclinical studies demonstrating the potential benefits of targeting the activities of these ligands have fueled the development of numerous biologics capable of perturbing this signaling pathway and increasing muscle mass and function. These biologics have been tested in numerous clinical trials for a wide range of indications characterized by muscle loss and excess adiposity. Here, we review the results of these trials and discuss some of the challenges and future prospects for targeting this signaling pathway to treat muscle and metabolic diseases. Myostatin inhibitors may improve metabolic outcomes by increasing muscle mass, and metabolic disorders may be attractive potential indications for these molecules.

Indexed as

Muscle, SkeletalMyostatinActivinsSignal TransductionTransforming Growth Factor betaactivin AActivinsMyostatinTransforming Growth Factor betaActivin AMetabolic dysfunctionMobility-disabilityMuscle lossMyostatin

Identifiers

PMID36738276
PMCPMC10272974
OpenAlexW4319164410

What OpenQuestion holds

Textmetadata
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.