研究表明，小鼠Atp6v0d2基因的失活，导致骨量显著增加，其主要原因为破骨细胞功能缺失和骨形成增加。
The study shows that the inactivation of gene Atp6v0d2 in mice results in dramatically increased bone mass due to defective osteoclasts as well as enhanced bone formation.
研究表明，小鼠Atp6v0d2基因的失活，导致骨量显著增加，其主要原因为破骨细胞功能缺失和骨形成增加。
The study shows that the inactivation of gene Atp6v0d2 in mice results in dramatically increased bone mass due to defective osteoclasts as well as enhanced bone formation.
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