Why the study?
Cardiac fibroblasts play a key role in heart fibrosis, but how their metabolism changes during this process remains unclear.
Targeting GPT2-mediated glutamate to α-ketoglutarate conversion in cardiac fibroblasts dampens excessive mitochondrial ATP production and prevents cardiac fibrosis under pressure-overload conditions.
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Should not yet change practice; leaves open MSC-EV–delivered miR-30c-5p as a potential antifibrotic strategy requiring clinical validation.
A 2026 study studied this question.
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