Evidence map›Paper›PMID 23769949›Full record

ReviewThe international journal of biochemistry & cell biology2013

Molecular mechanisms and signaling pathways of angiotensin II-induced muscle wasting: potential therapeutic targets for cardiac cachexia.

Tadashi Yoshida, A Michael Tabony, Sarah Galvez, William E Mitch, Yusuke Higashi, Sergiy Sukhanov, Patrice Delafontaine

Abstract readReview
In one paragraph

Review in The international journal of biochemistry & cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 4 pooled it
4.8field-weighted citation impact, top 4% 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

81 citing papers in PubMed, 4 syntheses or guidelines pooled it, 144 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026
    Review
  6. Review
  7. Article
  8. Review
  9. 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
  10. Article
  11. Review
  12. Article
  13. Article
  14. Analysis of Risk Factors for the Association of Sarcopenia in Patients with Type 2 Diabetes Mellitus.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Role of Endothelial Progenitor Cells in Frailty.International journal of molecular sciences · 2023
    Review
  20. Article

21 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 2 institutions in 1 country.

Tadashi YoshidaHeart and Vascular Institute, Tulane University School of Medicine, New Orleans, LA, United States.
A Michael Tabony
Sarah Galvez
William E Mitch
Yusuke Higashi
Sergiy Sukhanov
Patrice Delafontaine
Tulane University · USBaylor College of Medicine · US

Funding

Tracking & Evaluation CoreU54GM104940 · NIGMS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI JUDD E SHELLITO · 2012 to 2026
$69.1M
VASCULAR SMOOTH MUSCLE PLASTICITY IN NITRIC OXIDEP20RR018766 · NCRR · LSU HEALTH SCIENCES CENTER · PI SONGU-MIZE, EMEL · 2003 to 2011
$18.5M
Insulin-Like Growth Factor-1and AtherosclerosisR01HL070241 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI PATRICE DELAFONTAINE · 2003 to 2026
$10.1M
Translational Research in Hypertension and Renal BiologyP30GM103337 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI NAVAR, LUIS GABRIEL · 2012 to 2016
$5.8M
ANGIOTENSIN II, IGF-1 AND SKELETAL MUSCLE ATROPHYR01HL080682 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI DELAFONTAINE, PATRICE · 2007 to 2015
$3.3M
MENTORING IN CARDIOVASCULAR BIOLOGYP20GM103514 · NIGMS · LSU HEALTH SCIENCES CENTER · PI KAPUSTA, DANIEL R · 2012 to 2012
$2.0M
NCRR NIH HHS P20 RR018766NCRR NIH HHS P20-RR018766NHLBI NIH HHS R01 HL070241NHLBI NIH HHS R01-HL070241NHLBI NIH HHS R01 HL080682NHLBI NIH HHS R01-HL080682NIGMS NIH HHS P20 GM103514NIGMS NIH HHS P20-GM103514NIGMS NIH HHS P30 GM103337NIGMS NIH HHS P30-GM103337NIGMS NIH HHS U54 GM104940NIGMS NIH HHS U54-GM104940
6 · The paper itself

Abstract

Cachexia is a serious complication of many chronic diseases, such as congestive heart failure (CHF) and chronic kidney disease (CKD). Many factors are involved in the development of cachexia, and there is increasing evidence that angiotensin II (Ang II), the main effector molecule of the renin-angiotensin system (RAS), plays an important role in this process. Patients with advanced CHF or CKD often have increased Ang II levels and cachexia, and angiotensin-converting enzyme (ACE) inhibitor treatment improves weight loss. In rodent models, an increase in systemic Ang II leads to weight loss through increased protein breakdown, reduced protein synthesis in skeletal muscle and decreased appetite. Ang II activates the ubiquitin-proteasome system via generation of reactive oxygen species and via inhibition of the insulin-like growth factor-1 signaling pathway. Furthermore, Ang II inhibits 5' AMP-activated protein kinase (AMPK) activity and disrupts normal energy balance. Ang II also increases cytokines and circulating hormones such as tumor necrosis factor-α, interleukin-6, serum amyloid-A, glucocorticoids and myostatin, which regulate muscle protein synthesis and degradation. Ang II acts on hypothalamic neurons to regulate orexigenic/anorexigenic neuropeptides, such as neuropeptide-Y, orexin and corticotropin-releasing hormone, leading to reduced appetite. Also, Ang II may regulate skeletal muscle regenerative processes. Several clinical studies have indicated that blockade of Ang II signaling via ACE inhibitors or Ang II type 1 receptor blockers prevents weight loss and improves muscle strength. Thus the RAS is a promising target for the treatment of muscle atrophy in patients with CHF and CKD. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.

Indexed as

Angiotensin IIAnimalsCachexiaHeart DiseasesHumansMolecular Targeted TherapyMuscle, SkeletalMuscular AtrophySignal TransductionAngiotensin II5-aminoimidazole-4-carboxamide ribonucleotideACEagouti-related proteinAgRPAICARAMP-activated kinaseAMPKAng IIangiotensin-converting enzymeangiotensin IIAngiotensin IIangiotensin II type 1 receptorAT1RCachexiaCHFcongestive heart failureCongestive heart failurecorticotropin-releasing hormoneCRHend-stage renal diseaseERKESRDextracellular signal-regulted kinaseglucocorticoid receptorGRIGF-1IL-6insulin-like growth factor-1insulin receptor substarteinterleukin-6IRS-1mammalian target of rapamycinMAPKmitogen-activated kinasemTORneuropeptide YNpyphosphoinositide 3-kinasePI3KPOMCproopiomelanocortinreactive oxygen speciesROSSAAserum amyloid ASkeletal muscleTGF-βthyrotropin-releasing hormoneTNF-αtransforming growth factor-βTRHtumor necrosis factor-αubiquitin proteasome systemUPS

Identifiers

PMID23769949
PMCPMC3759646
OpenAlexW1972108813

What OpenQuestion holds

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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.