Evidence map›Paper›PMID 21282204›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011

Pharmacological inhibition of myostatin suppresses systemic inflammation and muscle atrophy in mice with chronic kidney disease.

Liping Zhang, Vik Rajan, Eugene Lin, Zhaoyong Hu, H Q Han, Xiaolan Zhou, Yanping Song, Hosung Min, Xiaonan Wang, Jie Du and 1 more

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 181 papers.

0numbers the graph read from it
0cells of the map it votes in
181citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

181 citing papers in PubMed, 300 citations in OpenAlex.

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121 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

11 authors at 3 institutions in 2 countries.

Liping ZhangNephrology Division, Baylor College of Medicine, Houston, Texas, USA 77030, USA.
Vik Rajan
Eugene Lin
Zhaoyong Hu
H Q Han
Xiaolan Zhou
Yanping Song
Hosung Min
Xiaonan Wang
Jie Du
William E Mitch
Baylor College of Medicine · USAmgen (United States) · USAtlanta University Center · US

Funding

Renal Inflammation: Mechanisms and ConsequencesP50DK064233 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MITCH, WILLIAM EVANS · 2003 to 2007
$5.1M
PROTEIN NUTRITION IN EXPERIMENTAL UREMIAR37DK037175 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MITCH, WILLIAM EVANS · 2006 to 2015
$3.8M
SMAD SIGNALING IN ANGIOTENSIN II-MEDIATED RENAL FIBROSISR01DK062828 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MITCH, WILLIAM EVANS · 2005 to 2006
$680k
NIDDK NIH HHS P50 DK064233NIDDK NIH HHS P50-DK64233NIDDK NIH HHS R01 DK062828NIDDK NIH HHS R01-DK62828NIDDK NIH HHS R37 DK037175NIDDK NIH HHS R37-DK37175
6 · The paper itself

Abstract

Chronic kidney disease (CKD) and several other catabolic conditions are characterized by increased circulating inflammatory cytokines, defects in IGF-1 signaling, abnormal muscle protein metabolism, and progressive muscle atrophy. In these conditions, no reliable treatments successfully block the development of muscle atrophy. In mice with CKD, we found a 2- to 3-fold increase in myostatin expression in muscle. Its pharmacological inhibition by subcutaneous injections of an anti-myostatin peptibody into CKD mice (IC(50) ∼1.2 nM) reversed the loss of body weight (≈5-7% increase in body mass) and muscle mass (∼10% increase in muscle mass) and suppressed circulating inflammatory cytokines vs. results from CKD mice injected with PBS. Pharmacological myostatin inhibition also decreased the rate of protein degradation (16.38 ± 1.29%; P<0.05), increased protein synthesis in extensor digitorum longus muscles (13.21 ± 1.09%; P<0.05), markedly enhanced satellite cell function, and improved IGF-1 intracellular signaling. In cultured muscle cells, TNF-α increased myostatin expression via a NF-κB-dependent pathway, whereas muscle cells exposed to myostatin stimulated IL-6 production via p38 MAPK and MEK1 pathways. Because IL-6 stimulates muscle protein breakdown, we conclude that CKD increases myostatin through cytokine-activated pathways, leading to muscle atrophy. Myostatin antagonism might become a therapeutic strategy for improving muscle growth in CKD and other conditions with similar characteristics.

Indexed as

AnimalsCell LineInsulin-Like Growth Factor IInterleukin-6Kidney DiseasesMaleMiceMice, Inbred C57BLMuscle, SkeletalMuscular AtrophyMyostatinNF-kappa BPolymerase Chain ReactionRecombinant Fusion ProteinsSignal TransductionInsulin-Like Growth Factor IInterleukin-6MyostatinNF-kappa BRecombinant Fusion Proteins

Identifiers

PMID21282204
PMCPMC3079306
OpenAlexW2085098316

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.