Why the study?
The mature mammalian heart has limited capacity for self-repair and regeneration.
PHGDH promotes cardiomyocyte proliferation and myocardial regeneration after cardiac injury by activating the cell cycle and TGF-β/Smad signaling pathways, offering a potential therapeutic target for heart repair.
May support PHGDH as a regeneration target in models; leaves open translation to human myocardial repair.
The mature mammalian heart has limited ability for self-repair and regeneration. Here, we establish phosphoglycerate dehydrogenase (PHGDH) as a crucial key for cardiomyocyte proliferation, with diminishing expression during postnatal cardiac development. PHGDH overexpression promoted myocardial regeneration and cardiac function in apical resection-operated mice, whereas inhibition by NCT-503 inhibited these processes. In vitro, PHGDH stimulated the proliferation of cardiomyocytes (CMs), while NCT-503 abolished its effect. Mechanistically, PHGDH activated the cell cycle and TGF-β/Smad signalling. Moreover, PHGDH significantly enhances cardiac repair and stimulates cardiomyocyte proliferation in adult mice following myocardial infarction. Our study demonstrates that upregulating PHGDH promotes CM proliferation and myocardial regeneration, offering a promising therapeutic target for myocardial repair.
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Zhang et al. (2025) studied this question.
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