Sphingosine-1-phosphate (S1P) is an important biologically active sphingolipid catabolic metabolite that regulates a variety of cellular functions including cell migration, vascular cell proliferation, vascular tone, endothelial barrier integrity, and inflammation by binding to the S1P receptor (S1PR). Given that S1P signaling is associated with multiple immune processes, therapies targeting the S1P axis may be appropriate for the treatment of stroke. Data from experimental stroke models and clinical trials suggest that S1PR1 regulation improves endothelial health and function, thereby contributing to improved neurological outcomes after ischemic injury. S1PR is emerging as a relevant therapeutic target during ischemic stroke.
Fig. 1. S1P signaling pathway involved in ischemic stroke. (Zhang et al., 2021)
At Ace Therapeutics, our team of experts utilizes cutting-edge technology and state-of-the-art equipment to study the role of S1P signaling in the pathophysiology of stroke and develop S1P targeted therapeutic strategies for ischemic stroke.
S1P is emerging as a potent modulator of vascular integrity through its receptor S1PR. We offer genetic approaches and a wide range of in vitro and animal models of stroke to analyze the efficacy of S1PR modulators in treating stroke by detecting neuronal apoptosis, cerebral edema, infarct size, neurological deficits, astrocyte activity, T-lymphocyte counts, blood-brain barrier disruption, and inflammatory factor expression.
We can help clients develop more specific S1PR modulators and find other targets in the S1P signaling pathway for ischemic stroke.
Ace Therapeutics provides reliable services to investigate the role of S1P signaling in stroke. We work closely with clients to provide customized solutions to meet the unique requirements of each research project. If you are interested in our services, please do not hesitate to contact us!
Ace Therapeutics is a global leading provider of stroke research services. We are committed to accelerating progress in stroke research and drug development.