Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
September 19, 2022CirculationOpen Access

Proteasomal Degradation of TRAF2 Mediates Mitochondrial Dysfunction in Doxorubicin-Cardiomyopathy

View Full Paper
Ask AI
Bookmark
Share

Population

Cardiac myocytes

Authors

RDRimpy DhingraSt. Boniface HospitalIRInna Rabinovich-NikitinAgriculture and Agri-Food CanadaSRSonny RothmanSt. Boniface Hospital

Discussion

Loading...

Member takes

Overview

Does not alter doxorubicin use; leaves open TRAF2 as a cardioprotective target pending human studies.

Structured PICO

P
Population
Cardiac myocytes
I
Intervention
Doxorubicin (DOX)
O
Outcome
Proteasomal degradation of TRAF2 and TNFα-mediated necrotic cell deathsurrogate

The study identifies a novel mechanism of doxorubicin-induced cardiomyopathy involving TRAF2 degradation and subsequent sensitization to necrotic cell death.

Cite This Study

Dhingra et al. (2022) studied this question.

synapsesocial.com/papers/69deeea7488ed2d92be94483https://doi.org/10.1161/circulationaha.121.058411
View Full Paper
Ask AI
Bookmark
Share

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Generation and Evaluation of Isogenic iPSC as a Source of Cell Replacement Therapies in Patients with Kearns Sayre Syndrome2021 · 17 citations
  2. 2TNF receptor–activated factor 2 mediates cardiac protection through noncanonical NF-κB signaling2018 · 24 citations
  3. 3Plasma TNF-α and Soluble TNF Receptor Levels after Doxorubicin with or without Co-Administration of Mesna—A Randomized, Cross-Over Clinical Study2015 · 51 citations
  4. 4TRAF2 Controls Death Receptor-Induced Caspase-8 Processing and Facilitates Proinflammatory Signaling2019 · 22 citations
  5. 5Doxorubicin acts through tumor necrosis factor receptor subtype 1 to cause dysfunction of murine skeletal muscle2009 · 104 citations