Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
October 7, 2017AJP Heart and Circulatory PhysiologyOpen Access

HDL protects against doxorubicin-induced cardiotoxicity in a scavenger receptor class B type 1-, PI3K-, and Akt-dependent manner

View Full Paper
Ask AI
Bookmark
Share

Key result

Raising apoA1 to supraphysiological levels protected against doxorubicin-induced cardiotoxicity via a pathway mediated by SR-B1 and involving Akt1/2 activation.

Why the study?

Does increasing HDL levels protect against doxorubicin-induced cardiotoxicity in mice and cardiomyocytes?

Population

Transgenic mice with increased HDL levels, wild-type mice, SR-B1 knockout mice, primary neonatal mouse…

Comparison

Increased HDL levels through overexpression of… vs Wild-type mice with normal HDL levels treated…

Design

Preclinical

Authors

KDKristina K. DurhamMcMaster UniversityKCKevin M. ChathelyThrombosis and Atherosclerosis Research InstituteKMKei Cheng MakUniversity of Toronto

Discussion

Loading...

Member takes

Implication

May support apoA1-raising strategies against doxorubicin cardiotoxicity; hypothesis-generating for SR-B1/Akt translation in patients.

Structured PICO

Does increasing HDL levels protect against doxorubicin-induced cardiotoxicity in mice and cardiomyocytes?

P
Population
Transgenic mice overexpressing human apolipoprotein A1 and cultured cardiomyocytes exposed to doxorubicin.
I
Intervention
Increased HDL levels through overexpression of human apolipoprotein A1 (apoA1 Tg/Tg) prior to doxorubicin treatment.
C
Comparator
Wild-type mice (apoA1 +/+) with normal HDL levels treated with doxorubicin.
O
Outcome
Doxorubicin-induced cardiotoxicity (cardiac dysfunction, cardiomyocyte atrophy, and apoptosis).surrogate

Raising apoA1 to supraphysiological levels protects against doxorubicin-induced cardiotoxicity via a pathway mediated by SR-B1 and involving Akt1/2 activation.

Cite This Study

Durham et al. (2017) studied Doxorubicin-induced cardiotoxicity. Increased HDL levels (apoA1 overexpression) vs. Wild-type mice (normal HDL levels) was evaluated on Doxorubicin-induced cardiac dysfunction, cardiomyocyte atrophy, and apoptosis. Raising apoA1 to supraphysiological levels protected against doxorubicin-induced cardiotoxicity via a pathway mediated by SR-B1 and involving Akt1/2 activation.

synapsesocial.com/papers/6a237393fdd7df511fd312a6https://doi.org/10.1152/ajpheart.00521.2016
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. 1Preventive Effect of Erythropoietin on Cardiac Dysfunction in Doxorubicin-Induced Cardiomyopathy2006 · 197 citations
  2. 2Thrombopoietin Protects Against Doxorubicin-Induced Cardiomyopathy, Improves Cardiac Function, and Reversely Alters Specific Signalling Networks2011 · 32 citations
  3. 3Adriamycin cardiomyopathy: pathophysiology and prevention1997 · 310 citations
  4. 4Akt Activation Preserves Cardiac Function and Prevents Injury After Transient Cardiac Ischemia In Vivo2001 · 701 citations
  5. 5Abnormal lipoprotein metabolism and reversible female infertility in HDL receptor (SR-BI)–deficient mice2001 · 183 citations