TNF-α Mediated Alterations in Human Glomerular Microvascular Endothelial Cell Metabolism, Function and morphology: Implications for Therapeutic Strategies

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Tumor necrosis factor alpha (TNF-α) is a proinflammatory cytokine that plays a crucial role in various inflammatory conditions. Understanding how TNF-α alters the structure, metabolic profiles, and functional conditions of primary human glomerular microvascular endothelial cells may reveal mechanisms that could be targeted for therapeutic interventions. This study investigated the impact of TNF-α on HGMVECs by assessing its effects on HLA antigen expression, morphology, migration, proliferation, glycolytic flux, and mitochondrial respiration. TNF-α treatment upregulated HLA class I on HGMVECs, altered their morphology to more elongated shapes and impaired their migration and proliferation. TNF-α reduced both glycolytic and mitochondrial metabolic rates in HGMVECs, but the cell retain their ability to respond to metabolic stress through the OXPHOS pathway. These findings demonstrate that TNF-α induces significant changes in HGMVECs that, in vivo, could significantly disrupt vascular homeostasis and may contribute to glomerular functional alterations during inflammatory and renal transplant rejection states.

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