TRPV2 knockout mice demonstrate an improved cardiac performance following myocardial infarction due to attenuated activity of peri-infarct macrophages.
Michal Entin-MeerLena CohenEinat Hertzberg-BigelmanRan LevyJeremy Ben-ShoshanGad KerenPublished in: PloS one (2017)
The data suggest that knockout of the TRPV2 channel may attenuate macrophage-dependent pro-inflammatory processes and result in better cardiac recovery. TRPV2 may thus represent a novel therapeutic target for treatment of patients undergoing an acute MI.
Keyphrases
- left ventricular
- patients undergoing
- neuropathic pain
- heart failure
- acute myocardial infarction
- electronic health record
- adipose tissue
- respiratory failure
- drug induced
- big data
- spinal cord injury
- spinal cord
- intensive care unit
- artificial intelligence
- atrial fibrillation
- percutaneous coronary intervention
- mechanical ventilation