Direct neuronal protection by the protease-activated receptor PAR4 antagonist ML354 after experimental stroke in mice.
Michael FleischerRebecca D SzepanowskiValeria PesaraJulia Sophie BihoracBeatrice OehlerDobromir DobrevChristoph KleinschnitzAnke C FenderPublished in: British journal of pharmacology (2024)
Selective PAR4 inhibition during reperfusion improves infarct size and neurological function after experimental stroke by blunting neuronal excitability, apoptosis, and local inflammation. PAR4 antagonists may provide additional neuroprotective benefits in patients with acute stroke beyond their canonical antiplatelet action.
Keyphrases
- cerebral ischemia
- subarachnoid hemorrhage
- blood brain barrier
- oxidative stress
- brain injury
- atrial fibrillation
- endoplasmic reticulum stress
- acute myocardial infarction
- cell death
- cell cycle arrest
- type diabetes
- heart failure
- high fat diet induced
- coronary artery disease
- acute coronary syndrome
- cell proliferation
- adipose tissue
- percutaneous coronary intervention
- binding protein
- signaling pathway
- acute ischemic stroke