De Luca Francesco
Section of Endocrinology and Diabetes, St. Christopher's Hospital for Children, Department of Pediatrics, Drexel University College of Medicine, Philadelphia, Pennsylvania 19134, USA.
Pediatr Res. 2006 May;59(5):625-9. doi: 10.1203/01.pdr.0000214966.60416.1b.
In mammals, statural growth is primarily accomplished by endochondral ossification, which takes place at the growth plate. Growth plate chondrocyte proliferation, hypertrophy/differentiation, apoptosis, and cartilage matrix synthesis all contribute to chondrogenesis or cartilage formation, a process tightly coupled to the simultaneous remodeling of the cartilage into bone at the metaphyseal border of the growth plate. Growth plate chondrogenesis is regulated by the complex interaction of molecular signals acting systemically as well locally within the growth plate. This network is often dysregulated during chronic illnesses, thus resulting in impaired growth plate chondrogenesis and, in turn, growth failure. The principal events responsible for altered growth plate chondrogenesis in chronic illness are inflammation, protein/calorie deprivation, uremia/metabolic acidosis, glucocorticoids, and impaired GH/IGF-I axis.
在哺乳动物中，身高增长主要通过生长板处的软骨内成骨来实现。生长板软骨细胞的增殖、肥大/分化、凋亡以及软骨基质合成均有助于软骨形成，这一过程与生长板干骺端边界处软骨同时重塑为骨的过程紧密相关。生长板软骨形成受全身及生长板局部作用的分子信号复杂相互作用的调节。在慢性疾病期间，该网络常常失调，从而导致生长板软骨形成受损，进而造成生长障碍。导致慢性疾病中生长板软骨形成改变的主要因素包括炎症、蛋白质/热量缺乏、尿毒症/代谢性酸中毒、糖皮质激素以及生长激素/胰岛素样生长因子-Ⅰ轴受损。
