4.7 Article

Phosphatidylserine Supplementation as a Novel Strategy for Reducing Myocardial Infarct Size and Preventing Adverse Left Ventricular Remodeling

Journal

Publisher

MDPI
DOI: 10.3390/ijms22094401

Keywords

L-α -Phosphatidyl-L-serine; phosphatidylserine; myocardial infarction; cardio-protection; preconditioning; inflammation

Funding

  1. Interdisciplinary Centre for Clinical Research IZKF Aachen (junior research group)
  2. Clinician Scientist program of the Faculty of Medicine of the RWTH Aachen University
  3. Singapore Ministry of Health's National Medical Research Council under its Open FundYoung Individual Research Grant [NMRC/OFYIRG/0073/2018]
  4. National Health Innovation Centre Singapore [NHIC-I2S-1811007]
  5. SingHealth Duke-NUS Academic Medical Centre under its SingHealth Duke-NUS Academic Medicine Research Grant [AM/TP033/2020 [SRDUKAMR2033]]
  6. British Heart Foundation [CS/14/3/31002]
  7. Duke-NUS Signature Research Program - Ministry of Health
  8. Singapore Ministry of Health's National Medical Research Council [NMRC/CSA-SI/0011/2017, NMRC/CGAug16C006]
  9. COST (European Cooperation in Science and Technology) [CA16225]

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Phosphatidylserine has shown significant cardiomyocyte protection and improvement in heart function in both acute and chronic mouse models of myocardial infarction. The main mechanism of action seems to be through up-regulation of protein kinase C-epsilon. Additionally, pre-treatment with phosphatidylserine before AMI induction selectively inhibits neutrophil activation without affecting healing and fibrosis, suggesting a potential novel strategy for reducing infarct size and preventing myocardial injury.
Phosphatidylserines are known to sustain skeletal muscle activity during intense activity or hypoxic conditions, as well as preserve neurocognitive function in older patients. Our previous studies pointed out a potential cardioprotective role of phosphatidylserine in heart ischemia. Therefore, we investigated the effects of phosphatidylserine oral supplementation in a mouse model of acute myocardial infarction (AMI). We found out that phosphatidylserine increases, significantly, the cardiomyocyte survival by 50% in an acute model of myocardial ischemia-reperfusion. Similar, phosphatidylserine reduced significantly the infarcted size by 30% and improved heart function by 25% in a chronic model of AMI. The main responsible mechanism seems to be up-regulation of protein kinase C epsilon (PKC-epsilon), the main player of cardio-protection during pre-conditioning. Interestingly, if the phosphatidylserine supplementation is started before induction of AMI, but not after, it selectively inhibits neutrophil's activation, such as Interleukin 1 beta (IL-1 beta) expression, without affecting the healing and fibrosis. Thus, phosphatidylserine supplementation may represent a simple way to activate a pre-conditioning mechanism and may be a promising novel strategy to reduce infarct size following AMI and to prevent myocardial injury during myocardial infarction or cardiac surgery. Due to the minimal adverse effects, further investigation in large animals or in human are soon possible to establish the exact role of phosphatidylserine in cardiac diseases.

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