Evidence map›Paper›PMID 20046121›Full record

ReviewCritical care medicine2009

Sepsis-induced myopathy.

Leigh Ann Callahan, Gerald S Supinski

Open access · greenAbstract readReview
In one paragraph

Review in Critical care medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
158citing papers in PubMed, 2 pooled it
7.9field-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

158 citing papers in PubMed, 2 syntheses or guidelines pooled it, 289 citations in OpenAlex.

  1. Pooled it
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  17. Observational
  18. Arginine at the host-pathogen interface.Infection and immunity · 2025
    Review
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98 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.

Leigh Ann CallahanDivision of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, University of Kentucky, Lexington, KY, USA. lacall2@email.uky.edu
Gerald S Supinski
University of Kentucky HealthCare · US

Funding

MAPK/PKR Modulation of Diaphragm WeaknessR01HL081525 · NHLBI · UNIVERSITY OF KENTUCKY · PI SUPINSKI, GERALD S. · 2006 to 2010
$1.8M
FREE RADICALS AND MUSCLE DYSFUNCTION IN HEART FAILURER01HL063698 · NHLBI · UNIVERSITY OF ROCHESTER · PI SUPINSKI, GERALD S. · 2000 to 2005
$1.6M
Oxidant Mediated Diaphragm Dysfunction in DiabetesR01HL080609 · NHLBI · UNIVERSITY OF KENTUCKY · PI CALLAHAN, LEIGH A · 2006 to 2009
$1.4M
Caspase Mediated Diaphragmatic DysfunctionR01HL080429 · NHLBI · UNIVERSITY OF KENTUCKY · PI SUPINSKI, GERALD S. · 2006 to 2009
$1.4M
Diaphragm Mitochondrial Alterations in SepsisR01HL069821 · NHLBI · UNIVERSITY OF ROCHESTER · PI CALLAHAN, LEIGH A · 2001 to 2004
$1.3M
Evaluation and Treatment of Skeletal Muscle Weakness in Critically Ill PatientsRC1HL100239 · NHLBI · UNIVERSITY OF KENTUCKY · PI SUPINSKI, GERALD S. · 2009 to 2009
$481k
NHLBI NIH HHS HL 063698NHLBI NIH HHS HL 069821NHLBI NIH HHS HL 080429NHLBI NIH HHS HL 080609NHLBI NIH HHS HL 081525NHLBI NIH HHS R01 HL063698NHLBI NIH HHS R01 HL069821NHLBI NIH HHS R01 HL080429NHLBI NIH HHS R01 HL080609NHLBI NIH HHS R01 HL081525NHLBI NIH HHS RC1 HL100239
6 · The paper itself

Abstract

Sepsis is a major cause of morbidity and mortality in critically ill patients, and despite advances in management, mortality remains high. In survivors, sepsis increases the risk for the development of persistent acquired weakness syndromes affecting both the respiratory muscles and the limb muscles. This acquired weakness results in prolonged duration of mechanical ventilation, difficulty weaning, functional impairment, exercise limitation, and poor health-related quality of life. Abundant evidence indicates that sepsis induces a myopathy characterized by reductions in muscle force-generating capacity, atrophy (loss of muscle mass), and altered bioenergetics. Sepsis elicits derangements at multiple subcellular sites involved in excitation contraction coupling, such as decreasing membrane excitability, injuring sarcolemmal membranes, altering calcium homeostasis due to effects on the sarcoplasmic reticulum, and disrupting contractile protein interactions. Muscle wasting occurs later and results from increased proteolytic degradation as well as decreased protein synthesis. In addition, sepsis produces marked abnormalities in muscle mitochondrial functional capacity and when severe, these alterations correlate with increased death. The mechanisms leading to sepsis-induced changes in skeletal muscle are linked to excessive localized elaboration of proinflammatory cytokines, marked increases in free-radical generation, and activation of proteolytic pathways that are upstream of the proteasome including caspase and calpain. Emerging data suggest that targeted inhibition of these pathways may alter the evolution and progression of sepsis-induced myopathy and potentially reduce the occurrence of sepsis-mediated acquired weakness syndromes.

Indexed as

AnimalsCritical IllnessCytokinesFree RadicalsHumansMuscle Fibers, SkeletalMuscle ProteinsMuscle, SkeletalMuscular AtrophyMuscular DiseasesSepsisCytokinesFree RadicalsMuscle Proteins

Identifiers

PMID20046121
PMCPMC3967515
OpenAlexW1980424395

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.