Evidence map›Paper›PMID 21356358›Full record

ArticleThe American journal of pathology2011

NF-κB inhibition protects against tumor-induced cardiac atrophy in vivo.

Ashley Wysong, Marion Couch, Scott Shadfar, Luge Li, Lugi Li, Jessica E Rodriguez, Scott Asher, Xiaoying Yin, Mitchell Gore, Al Baldwin and 2 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Cardiac wasting in patients with cancer.Basic research in cardiology · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Advanced cancer is also a heart failure syndrome: a hypothesis.Journal of cachexia, sarcopenia and muscle · 2021
    Review
  11. Review
  12. Article
  13. Inter-tissue communication in cancer cachexia.Nature reviews. Endocrinology · 2018
    Review
  14. Article
  15. Molecular mechanism of sarcopenia and cachexia: recent research advances.Pflugers Archiv : European journal of physiology · 2017
    Review
  16. Article
  17. Article
  18. Article
  19. Pay attention to cardiac remodeling in cancer cachexia.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2016
    Review
  20. Review
4 · The record

Corrections and comments

  • Erratum issued
    Li, Lugi [corrected to Li, Luge]
5 · Who and what money

Authors and funding

12 authors at 2 institutions in 3 countries.

Ashley WysongDuke University School of Medicine, Durham, North Carolina, USA.
Marion Couch
Scott Shadfar
Luge Li
Lugi Li
Jessica E Rodriguez
Scott Asher
Xiaoying Yin
Mitchell Gore
Al Baldwin
Cam Patterson
Monte S Willis
University of North Carolina at Chapel Hill · USDuke University · US

Funding

Myocyte Signaling and the Response to StressR37HL065619 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PATTERSON, WINSTON C · 2010 to 2019
$3.7M
CHIP: A link between the chaperone &proteasome systemsR01GM061728 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SCHISLER, JONATHAN C. · 2001 to 2013
$3.4M
Myocyte specific regulation of metabolism and the response to biomechanical forceR01HL104129 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WILLIS, MONTE S · 2010 to 2018
$3.3M
Howard Hughes Medical InstituteNHLBI NIH HHS R01 HL104129NHLBI NIH HHS R01HL104129NHLBI NIH HHS R37 HL065619NIGMS NIH HHS R01 GM061728
6 · The paper itself

Abstract

Cancer cachexia is a severe wasting syndrome characterized by the progressive loss of lean body mass and systemic inflammation. It occurs in approximately 80% of patients with advanced malignancy and is the cause of 20% to 30% of all cancer-related deaths. The mechanism by which striated muscle loss occurs is the tumor release of pro-inflammatory cytokines, such as IL-1, IL-6, and TNF-α. These cytokines interact with their cognate receptors on muscle cells to enhance NF-κB signaling, which then mediates muscle loss and significant cardiac dysfunction. Genetic inhibition of NF-κB signaling has demonstrated its predominant role in skeletal muscle loss. Therefore, we tested two novel drugs designed to specifically inhibit NF-κB by targeting the IκB kinase (IKK) complex: Compound A and NEMO binding domain (NBD) peptide. Using an established mouse model of cancer cachexia (C26 adenocarcinoma), we determined how these drugs affected the development of tumor-induced cardiac atrophy and function. Echocardiographic and histological analysis revealed that both Compound A and NBD inhibit cardiac NF-κB activity and prevent the development of tumor-induced systolic dysfunction and atrophy. This protection was independent of any effects of the tumor itself (Compound A) or tumor-secreted cytokines (NBD). This study identifies for the first time, to our knowledge, that drugs targeting the IKK complex are cardioprotective against cancer cachexia-induced cardiac atrophy and systolic dysfunction, suggesting therapies that may help reduce cardiac-associated morbidities found in patients with advanced malignancies.

Indexed as

AdenocarcinomaAnimalsAtrophyCachexiaCardiotonic AgentsCell SizeCytokinesMiceMice, Inbred BALB CMuscle ProteinsMyocardiumMyocytes, CardiacNeoplasm TransplantationNF-kappa BOrgan SizePeptidesCardiotonic AgentsCytokinesFbxo32 protein, mouseMuscle ProteinsNBD peptide, mouseNF-kappa BPeptidesSKP Cullin F-Box Protein LigasesTrim63 protein, mouseTripartite Motif ProteinsUbiquitin-Protein Ligases

Identifiers

PMID21356358
PMCPMC3070568
OpenAlexW2072805739

What OpenQuestion holds

Textmetadata
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.