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October 8, 2013Journal of Translational MedicineOpen Access

Notch signaling activation contributes to cardioprotection provided by ischemic preconditioning and postconditioning

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Key result

Notch1 signaling is activated during ischemic preconditioning and postconditioning, and its activation mediates cardioprotection by reducing infarct size and improving cardiac function.

Why the study?

Does lentiviral overexpression of N1ICD improve cardioprotection (cell viability, infarct size, cardiac function) in rat cardiomyocytes and isolated hearts exposed to ischemia/reperfusion injury?

Population

Rat cardiac H9c2 cells and male Sprague-Dawley rats exposed to ischemia/reperfusion injury, ischemic…

Comparison

Lentiviral vectors to overexpress or knockdown… vs Empty vector, non-specific sequence vector, and…

Design

Preclinical

Follow-up

120 minutes of reperfusion (Langendorff model)

Authors

XZXueliang ZhouLWLi WanQXQirong Xu

Discussion

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Member takes

Overview

Notch1 activation may offer a target for cardioprotection in ischemia; animal data leave open clinical translation.

Structured PICO

Does lentiviral overexpression of N1ICD improve cardioprotection (cell viability, infarct size, cardiac function) in rat cardiomyocytes and isolated hearts exposed to ischemia/reperfusion injury?

P
Population
In vitro H9c2 cardiomyocytes and ex vivo male Sprague-Dawley rat hearts subjected to ischemia/reperfusion injury, ischemic preconditioning, and ischemic postconditioning.
I
Intervention
Lentiviral vectors to overexpress or knockdown N1ICD (Notch1 intracellular domain).
C
Comparator
Empty vector (Mock1), non-specific sequence vector (Mock2), and standard ischemia/reperfusion without pre/post-conditioning.
O
Outcome
Cell viability, apoptosis, mitochondrial membrane potential, reactive oxygen species, cardiac function (LVDP, HR, ±dP/dt), lactate dehydrogenase (LDH) release, and infarct size.surrogate

Main Result

p-value: p=<0.05

Notch1 signaling is activated during and mediates the cardioprotective effects of ischemic preconditioning and postconditioning, highlighting it as a potential pharmacological target for ischemic heart disease.

Limitations

  • Animal and cell models may not fully translate to human ischemic heart disease

Cite This Study

Zhou et al. (2013) studied Myocardial ischemia reperfusion injury. Notch1 signaling activation (N1ICD overexpression) or knockdown vs. Control/Mock vectors and Ischemia/Reperfusion alone was evaluated on Cardioprotection (infarct size, cardiac function, cell viability, apoptosis) (p=<0.05). Notch1 signaling is activated during ischemic preconditioning and postconditioning, and its activation mediates cardioprotection by reducing infarct size and improving cardiac function.

synapsesocial.com/papers/6a9bbde7092f20adc69814c8https://doi.org/10.1186/1479-5876-11-251
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Also Consider

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

  1. 1Reperfusion Injury Salvage Kinase and Survivor Activating Factor Enhancement Prosurvival Signaling Pathways in Ischemic Postconditioning: Two Sides of the Same Coin2010 · 186 citations
  2. 2Cardioprotection by Ischemic Postconditioning Is Lost in Aged and STAT3-Deficient Mice2007 · 275 citations
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  4. 4Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning2003 · 2,049 citations
  5. 5Canonical notch pathway protects hepatocytes from ischemia/reperfusion injury in mice by repressing reactive oxygen species production through JAK2/STAT3 signaling2011 · 118 citations