Molecular mechanisms of neuroprotective effects of thyroid hormones and their metabolites in acute brain ischemia

Abstract

As endovascular reperfusion advances and multimodal neuroimagimg is implemented, neuroprotection in ischemic stroke progresses to the next level. In the recent years, the focus of neuroprotection research has been gradually shifting towards the research of endogenous substances and their synthetic analogs. According to the available evidence, thyroid hormones (THs) and their metabolites are potentially effective neuroprotectors in brain ischemia.
 Objective. To identify and classify TH neuroprotective effects in acute brain ischemia by analyzing contemporary data.
 We studied and analyzed publications indexed in РubMed, SciElo, ScienceDirect, Scopus, Biomedical Data Journal, and eLibrary.
 The molecular basis of TH effects includes genomic and non-genomic mechanisms aimed at mitochondrial activity regulation, neuro- and angiogenesis, axonal transport, cytoskeleton maintenance, and impact on ion channels as well as activation and expression of specific proteins. TH effects on the central nervous system can be classified into following clusters: influence on neuronal and glial metabolism, apoptosis modulation, neuroplasticity and angiogenesis, impact on hemostasis, and local and systemic immune response.
 Conclusion. THs are multimodal and selective regulators of cellular processes that affect neuroplasticity and neuro-reintegration both in the brain ischemic zone and beyond it. Therefore, a promising research can cover THs and and their metabolites as cerebral cytoprotectors to improve functional outcomes of ischemic strokes.