Evidence map›Paper›PMID 23154422›Full record

ReviewBiological chemistry2013

Mitochondrial pathways in sarcopenia of aging and disuse muscle atrophy.

Riccardo Calvani, Anna-Maria Joseph, Peter J Adhihetty, Alfredo Miccheli, Maurizio Bossola, Christiaan Leeuwenburgh, Roberto Bernabei, Emanuele Marzetti

Open access · bronzeAbstract readReview
In one paragraph

Review in Biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 177 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
177citing papers in PubMed, 1 pooled it
6.8field-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

177 citing papers in PubMed, 1 synthesis or guideline pooled it, 313 citations in OpenAlex.

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117 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

8 authors at 5 institutions in 2 countries.

Riccardo CalvaniInstitute of Crystallography, Italian National Research Council (CNR), Bari 70126, Italy.
Anna-Maria Joseph
Peter J Adhihetty
Alfredo Miccheli
Maurizio Bossola
Christiaan Leeuwenburgh
Roberto Bernabei
Emanuele Marzetti
Università Cattolica del Sacro Cuore · ITInstitute on Aging · USNational Research Council · ITSapienza University of Rome · ITUniversity of Florida · US

Funding

University of Florida Older Americans Independence Center (OAIC)P30AG028740 · NIA · UNIVERSITY OF FLORIDA · PI CHRISTIAAN LEEUWENBURGH · 2007 to 2026
$22.8M
Apoptosis and Life-Long Caloric RestrictionR01AG021042 · NIA · UNIVERSITY OF FLORIDA · PI LEEUWENBURGH, CHRISTIAAN · 2003 to 2007
$1.7M
Mitophagy: target to improve liver function after ischemia/reperfusion injuryR01DK090115 · NIDDK · UNIVERSITY OF FLORIDA · PI KIM, JAE-SUNG, LEEUWENBURGH, CHRISTIAAN · 2012 to 2015
$1.3M
NIA NIH HHS 1P30AG028740NIA NIH HHS P30 AG028740NIA NIH HHS R01 AG021042NIA NIH HHS R01-AG21042NIDDK NIH HHS R01 DK090115NIDDK NIH HHS R01-DK090115-01A1
6 · The paper itself

Abstract

Muscle loss during aging and disuse is a highly prevalent and disabling condition, but knowledge about cellular pathways mediating muscle atrophy is still limited. Given the postmitotic nature of skeletal myocytes, the maintenance of cellular homeostasis relies on the efficiency of cellular quality control mechanisms. In this scenario, alterations in mitochondrial function are considered a major factor underlying sarcopenia and muscle atrophy. Damaged mitochondria are not only less bioenergetically efficient, but also generate increased amounts of reactive oxygen species, interfere with cellular quality control mechanisms, and display a greater propensity to trigger apoptosis. Thus, mitochondria stand at the crossroad of signaling pathways that regulate skeletal myocyte function and viability. Studies on these pathways have sometimes provided unexpected and counterintuitive results, which suggests that they are organized into a complex, heterarchical network that is currently insufficiently understood. Untangling the complexity of such a network will likely provide clinicians with novel and highly effective therapeutics to counter the muscle loss associated with aging and disuse. In this review, we summarize the current knowledge on the mechanisms whereby mitochondrial dysfunction intervenes in the pathogenesis of sarcopenia and disuse atrophy, and highlight the prospect of targeting specific processes to treat these conditions.

Indexed as

HumansMitochondriaMuscular Disorders, AtrophicOxidative StressSarcopeniaSignal Transduction

Identifiers

PMID23154422
PMCPMC3976204
OpenAlexW2091503455

What OpenQuestion holds

Textmetadata
LicenceTDM
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.