October 6, 2005Journal of Biological ChemistryOpen Access

Poly(ADP-ribose) Polymerase-1-dependent Cardiac Myocyte Cell Death during Heart Failure Is Mediated by NAD+ Depletion and Reduced Sir2α Deacetylase Activity

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Structured PICO

Population

Failing hearts and cultured cardiac myocytes

Intervention

NAD repletion (adding NAD directly to the culture medium or by overexpressing NAD biosynthetic enzymes)

Outcome

Myocyte cell death induced by PARP activationsurrogate

In stressed cardiac myocytes, depletion of cellular NAD levels links PARP activation to reduced Sir2alpha deacetylase activity, contributing to myocyte cell death during heart failure.

Discussion

No takes yet. Share an insight, caveat, or question.

Implication

Should not yet change practice in heart failure; leaves open Sir2alpha-dependent NAD pathways for future investigation.

Cite This Study

Pillai et al. (2005) studied this question.

synapsesocial.com/papers/69df12e73b0ba53fb37a1205 https://doi.org/10.1074/jbc.m506162200

Topics

Heart failure HFrEF treatment

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Poly(ADP-ribose) Polymerase-1-dependent Cardiac Myocyte Cell Death during Heart Failure Is Mediated by NAD+ Depletion and Reduced Sir2α Deacetylase Activity

Structured PICO

Discussion

Implication

Cite This Study

Topics

Poly(ADP-ribose) Polymerase-1-dependent Cardiac Myocyte Cell Death during Heart Failure Is Mediated by NAD+ Depletion and Reduced Sir2α Deacetylase Activity

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Topics

Also Consider