Abstract
Lipid-accumulated reactive astrocytes (LARAs) have recently been confirmed to be a pivotal cell type present in temporal lobe epilepsy (TLE) lesions. These cells not only induce anomalous lipid accumulation within the epileptic foci but also decrease the seizure threshold by employing upregulated activation of the adenosine A2A receptor (A2AR). Furthermore, disturbances in mitochondrial oxidative phosphorylation (OxPhos) have been noted as significant drivers of lipid accumulation in astrocytes. Moreover, the deficiency of OxPhos in astrocytes can induce severe neuroinflammation, which can worsen the progression of TLE. Accordingly, further exploration of the correlation between mitochondrial dysfunction, LARAs-mediated lipid accumulation, and A2AR activation within epilepsy lesions is warranted. It could potentially elucidate the vital role of mitochondrial dysfunction in the pathogenesis of TLE.
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