Evidence map›Paper›PMID 21747283›Full record

ReviewThe American journal of the medical sciences2011

Angiotensin II, oxidative stress and skeletal muscle wasting.

Sergiy Sukhanov, Laura Semprun-Prieto, Tadashi Yoshida, A Michael Tabony, Yusuke Higashi, Sarah Galvez, Patrice Delafontaine

Abstract readReview
In one paragraph

Review in The American journal of the medical sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 2 pooled it
6.1field-weighted citation impact, top 3% 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

72 citing papers in PubMed, 2 syntheses or guidelines pooled it, 153 citations in OpenAlex.

  1. Low dialysate sodium levels for chronic haemodialysis.The Cochrane database of systematic reviews · 2024
    Pooled it
  2. Low dialysate sodium levels for chronic haemodialysis.The Cochrane database of systematic reviews · 2019
    Pooled it
  3. Article
  4. Review
  5. Review
  6. Review
  7. Targeting MuRF1 to Combat Skeletal Muscle Wasting in Cardiac Cachexia: Mechanisms and Therapeutic Prospects.Medical science monitor : international medical journal of experimental and clinical research · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Circulating Cell-Free Mitochondrial DNA: A Potential Blood-Based Biomarker for Sarcopenia in Patients Undergoing Maintenance Hemodialysis.Medical science monitor : international medical journal of experimental and clinical research · 2022
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. ACE2, angiotensin 1-7 and skeletal muscle: review in the era of COVID-19.Clinical science (London, England : 1979) · 2020
    Review

12 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

7 authors at 1 institution in 1 country.

Sergiy SukhanovTulane University Heart and Vascular Institute, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Laura Semprun-Prieto
Tadashi Yoshida
A Michael Tabony
Yusuke Higashi
Sarah Galvez
Patrice Delafontaine
Tulane University · US

Funding

Insulin-Like Growth Factor-1and AtherosclerosisR01HL070241 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI PATRICE DELAFONTAINE · 2003 to 2026
$10.1M
ANGIOTENSIN II, IGF-1 AND SKELETAL MUSCLE ATROPHYR01HL080682 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI DELAFONTAINE, PATRICE · 2007 to 2015
$3.3M
NHLBI NIH HHS R01 HL070241NHLBI NIH HHS R01 HL080682
6 · The paper itself

Abstract

Muscle atrophy (cachexia) is a muscle wasting syndrome associated with several pathological conditions in humans such as congestive heart failure, diabetes, AIDS, cancer and renal failure, and the presence of cachexia worsens outcome. Many of the conditions associated with cachexia are accompanied by stimulation of the renin-angiotensin system and elevation in angiotensin II (ang II) levels. Ang II infusion induces skeletal muscle atrophy in rodents and mechanisms include increased expression of the E3 ligases atrogin-1/MuRF-1, an elevated rate of ubiquitin-proteasome mediated proteolysis and increased reactive oxygen species (ROS) levels, closely mimicking conditions of human cachexia. Ang II-induced oxidative stress contributes to muscle atrophy in a mouse model. Nicotinamide adenine dinucleotide phosphate oxidase- and mitochondria-derived ROS contribute to ang II-induced oxidative stress. Specific targeting of ROS and nicotinamide adenine dinucleotide phosphate oxidase/mitochondria cross-talk could be a beneficial, novel therapy to treat cachexia.

Indexed as

Angiotensin IIAnimalsHumansMiceMitochondria, MuscleMuscular AtrophyNADPH OxidasesOxidative StressReactive Oxygen SpeciesReceptors, AngiotensinAngiotensin IINADPH OxidasesReactive Oxygen SpeciesReceptors, Angiotensin

Identifiers

PMID21747283
PMCPMC3217236
OpenAlexW1973595217

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.