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August 10, 2007Journal of Clinical InvestigationOpen Access

TNF provokes cardiomyocyte apoptosis and cardiac remodeling through activation of multiple cell death pathways

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Why the study?

Does cardiac-restricted overexpression of Bcl-2 prevent adverse cardiac remodeling and cardiomyocyte apoptosis in transgenic mice with cardiac-restricted overexpression of TNF?

Population

Transgenic mice with cardiac-restricted overexpression of secretable TNF (MHCsTNF)

Comparison

Cardiac-restricted overexpression of Bcl-2 vs MHCsTNF mice without Bcl-2 overexpression

Design

Preclinical

Authors

SHSandra B. HaudekBaylor College of MedicineGTGeorge E. TaffetHeart Failure & TransplantMSMichael SchneiderKarlsruhe Institute of Technology

Discussion

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Implication

Bcl-2 overexpression alone insufficient to block TNF-driven apoptosis in mice; hypothesis-generating for multi-pathway targeting in inflammatory cardiomyopathy.

Structured PICO

Does cardiac-restricted overexpression of Bcl-2 prevent adverse cardiac remodeling and cardiomyocyte apoptosis in transgenic mice with cardiac-restricted overexpression of TNF?

P
Population
Transgenic mice with cardiac-restricted overexpression of secretable TNF (MHCsTNF)
I
Intervention
Cardiac-restricted overexpression of Bcl-2 (via crossing MHCsTNF mice with transgenic mice harboring cardiac-restricted overexpression of Bcl-2)
C
Comparator
MHCsTNF mice without Bcl-2 overexpression
O
Outcome
Adverse cardiac remodeling (LV wall thinning) and cardiomyocyte apoptosissurrogate

Sustained TNF-induced inflammation activates multiple cell death pathways in cardiomyocytes, and blocking the intrinsic pathway alone with Bcl-2 is insufficient to fully prevent apoptosis, highlighting the complexity of adverse cardiac remodeling.

Cite This Study

Haudek et al. (2007) studied this question.

synapsesocial.com/papers/69d89965a5ecc596b5d17cb8https://doi.org/10.1172/jci29134
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