Interview with Liang Sijia, a young scholar at Sun Yat-sen University: NFATc3, a potential therapeutic target for inhibiting atherosclerosis

Professor Liang Sijia of Zhongshan Medical College is committed to the study of the pathogenesis mechanism of metabolic cardiovascular diseases, especially cardiovascular-related diseases induced by hyperlipidemia, and systematically studied the pathological significance

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Teacher Liang: Our team has been doing systematic research on ion channels and metabolic cardiovascular diseases, and in the early work of studying the relationship between calcium signaling and atherosclerosis, it was found that calcium ion inflow mediated by calcium pool manipulation calcium channels can promote the occurrence

Regarding the adverse effects of the above immunosuppressant applications, whether they are directly related to the suppression of Calcineurin-NFAT is not known

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Teacher Liang: We know that macrophage foaming is a key factor in atherosclerotic plaque formation, its importance in atherosclerotic formation, and their enrichment within the plaque, making macrophages a promising therapeutic target for

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Teacher Liang: The purpose of constructing a mouse model of macrophage-specific overexpression of NFATc3 gene is to explore whether macrophages overexpress NFATc3 genes can produce phenotype effects that match macrophage-specific knockout NFATc3, so as to verify the key role

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Teacher Liang: We found in our study that simple knockout or high expression of macrophage NFATc3 does not affect the occurrence and development of atherosclerosis, which means that macrophage knockout NFATc3 does not spontaneously atherosclerosis

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Teacher Liang: We believe that from the perspective of basic research, it is proved that the NFATc3/miR-204 axis is a key factor

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Sijia Liang, Associate Professor

Xiaofeng Yu is vice president and chief scientist