Publications by authors named "Cindy X Li"
As the leading cause of mortality worldwide, cardiovascular disease (CVD) represents a variety of heart diseases and vascular disorders, including atherosclerosis, aneurysm, ischemic injury in the heart and brain, arrythmias, and heart failure. Macrophages, a diverse population of immune cells that can promote or suppress inflammation, have been increasingly recognized as a key regulator in various processes in both healthy and disease states. In healthy conditions, these cells promote the proper clearance of cellular debris, dead and dying cells, and provide a strong innate immune barrier to foreign pathogens.
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- The study explores how NMDAR-mediated glutamate excitotoxicity is a major cause of cell death in ischemic stroke, highlighting the failure of past treatments targeting NMDARs in clinical trials.
- Researchers discovered a specific interaction between TRPM2 and PKCγ that contributes to the excitotoxic process, proposing that breaking this interaction could be a new therapeutic approach.
- By developing a peptide (TAT-M2PBM) to disrupt the TRPM2-PKCγ coupling, the study shows that this uncoupling reduces calcium influx and excitotoxic effects, ultimately protecting neurons from ischemic damage.
Ischemic stroke is a devastating disease that affects millions of patients worldwide. Unfortunately, there are no effective medications for mitigating brain injury after ischemic stroke. TRP channels are evolutionally ancient biosensors that detect external stimuli as well as tissue or cellular injury.
View Article and Find Full Text PDFAims: Damage of the blood-brain barrier (BBB) is a hallmark of brain injury during the early stages of ischemic stroke. The subsequent endothelial hyperpermeability drives the initial pathological changes and aggravates neuronal death. Transient receptor potential melastatin 2 (TRPM2) is a Ca2+-permeable nonselective cation channel activated by oxidative stress.
View Article and Find Full Text PDFContext: Idiopathic hypogonadotropic hypogonadism (IHH) results from defective synthesis, secretion, or action of GnRH. Kisspeptin is a potent stimulus for GnRH secretion.
Objective: We probed the functional capacity of the GnRH neuronal network in patients with IHH.