Evidence map›Paper›PMID 24959824›Full record

ArticlePloS one2014

Haptoglobin is required to prevent oxidative stress and muscle atrophy.

Enrico Bertaggia, Gaia Scabia, Stefania Dalise, Francesca Lo Verso, Ferruccio Santini, Paolo Vitti, Carmelo Chisari, Marco Sandri, Margherita Maffei

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
3.0field-weighted citation impact, top 9% 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

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 71 citations in OpenAlex.

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  18. Saffron (Nutrients · 2022
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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 5 institutions in 1 country.

Enrico BertaggiaDepartment of Biomedical Sciences, University of Padova, Padova, Italy; Dulbecco Telethon Institute at Venetian Institute of Molecular Medicine, Padova, Italy.
Gaia ScabiaDepartment of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Stefania DaliseUnit of Neurorehabilitation, Department of Neuroscience, University Hospital of Pisa, Pisa, Italy.
Francesca Lo VersoDepartment of Biomedical Sciences, University of Padova, Padova, Italy; Dulbecco Telethon Institute at Venetian Institute of Molecular Medicine, Padova, Italy.
Ferruccio SantiniDepartment of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Paolo VittiDepartment of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Carmelo ChisariUnit of Neurorehabilitation, Department of Neuroscience, University Hospital of Pisa, Pisa, Italy.
Marco SandriDepartment of Biomedical Sciences, University of Padova, Padova, Italy; Dulbecco Telethon Institute at Venetian Institute of Molecular Medicine, Padova, Italy; CNR Institute of Neuroscience, Padova, Italy; Telethon Institute of Genetics and Medicine (TIGEM), Napoli, Italy.
Margherita MaffeiDepartment of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy; CNR Institute of Clinical Physiology, Pisa, Italy.
University of Pisa · ITAzienda Ospedaliera Universitaria Pisana · ITVeneto Institute of Molecular Medicine · ITIstituto di Fisiologia Clinica · ITUniversity of Padua · IT

Funding

Telethon TCR09003
6 · The paper itself

Abstract

backgroundOxidative stress (OS) plays a major role on tissue function. Several catabolic or stress conditions exacerbate OS, inducing organ deterioration. Haptoglobin (Hp) is a circulating acute phase protein, produced by liver and adipose tissue, and has an important anti-oxidant function. Hp is induced in pro-oxidative conditions such as systemic inflammation or obesity. The role of systemic factors that modulate oxidative stress inside muscle cells is still poorly investigated.

resultsWe used Hp knockout mice (Hp-/-) to determine the role of this protein and therefore, of systemic OS in maintenance of muscle mass and function. Absence of Hp caused muscle atrophy and weakness due to activation of an atrophy program. When animals were stressed by acute exercise or by high fat diet (HFD), OS, muscle atrophy and force drop were exacerbated in Hp-/-. Depending from the stress condition, autophagy-lysosome and ubiquitin-proteasome systems were differently induced.

conclusionsHp is required to prevent OS and the activation of pathways leading to muscle atrophy and weakness in normal condition and upon metabolic challenges.

Indexed as

Oxidative StressAnimalsAutophagyDiet, High-FatGene ExpressionHaptoglobinsLysosomesMaleMice, KnockoutMitochondriaMuscular AtrophyObesityOxidation-ReductionPhysical Conditioning, AnimalProteasome Endopeptidase ComplexSignal TransductionHaptoglobinsProteasome Endopeptidase ComplexUbiquitin

Identifiers

PMID24959824
PMCPMC4069100
OpenAlexW1996201543

What OpenQuestion 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 OpenQuestion graph.