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May 8, 2018Journal of Cellular Biochemistry

Notch signaling promotes angiogenesis and improves cardiac function after myocardial infarction

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Population

Cultured human umbilical vein endothelial cells exposed to hypoxia/reoxygenation and myocardial infarction…

Comparison

Overexpression or knockdown of Notch… vs Control conditions

Design

Preclinical

Authors

XZXueliang ZhouRZRongrong ZhuSLSheng Liu

Discussion

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Overview

Does not support Notch modulation in MI care; leaves open its endothelial role pending in vivo studies.

Structured PICO

P
Population
Cultured human umbilical vein endothelial cells (HUVECs) exposed to hypoxia/reoxygenation (H/R) and myocardial infarction (MI) model rats
I
Intervention
Overexpression or knockdown of Notch intracellular domain (NICD)
C
Comparator
Control conditions
O
Outcome
Cell proliferation, VEGF secretion, and tube formation (in vitro); heart dysfunction and angiogenesis (in vivo)surrogate

Activation of Notch signaling promotes angiogenesis and improves cardiac function following myocardial infarction in preclinical models.

Cite This Study

Zhou et al. (2018) studied this question.

synapsesocial.com/papers/6a79573f756812e39588ff00https://doi.org/10.1002/jcb.27032
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Also Consider

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

  1. 1Notch signaling activation contributes to cardioprotection provided by ischemic preconditioning and postconditioning2013 · 64 citations
  2. 2Notch1 in Bone Marrow–Derived Cells Mediates Cardiac Repair After Myocardial Infarction2011 · 85 citations
  3. 3Role of Notch signaling in the mammalian heart2013 · 52 citations
  4. 4The Biological Basis for Cardiac Repair After Myocardial Infarction2016 · 2,282 citations
  5. 5Salidroside suppressing <scp>LPS</scp>‐induced myocardial injury by inhibiting <scp>ROS</scp>‐mediated <scp>PI</scp>3K/Akt/<scp>mTOR</scp> pathway <i>in vitro</i> and <i>in vivo</i>2017 · 254 citations