Okay, so chondrocytes are important for the articular cartilage, got it.

因此软骨细胞对关节软骨非常重要。

So an osteoblast in your bone becomes an osteocyte — ditto for chondroblasts becoming chondrocytes.

所以你骨骼中成骨细胞就变成了一个骨细胞。——软骨母细胞成为软骨细胞也是如此。

Chondrosarcoma arises from the chondrocytes which are cartilage-producing cells.

软骨肉瘤起源于软骨细胞，即产生软骨细胞。

Whatever the initial cause of articular cartilage damage is, it gets the chondrocytes to start trying to repair the cartilage.

不管引起关节软骨损伤起始因素是什，有软骨细胞开始尝试修复软骨。

These plates increase the length of your bones through proliferation of ossifying cells we call chondrocytes.

这些骨骺板通过骨化细胞增殖增加骨骼长度，们称之为软骨细胞。

Maintaining healthy articular cartilage is the chondrocyte's job, a specialized cell responsible for maintaining everything cartilage-related.

保持关节软骨健康是软骨细胞工作；软骨细胞是负责一切软骨相关特殊细胞。

Results FOS-positive chondrocytes were increased in human and murine OA cartilage during disease progression.

结果显示，在疾病进展过程中，人类和小鼠OA软骨中FOS阳性软骨细胞增多。

Chondrocytes lacking c-Fos proliferate less, have shorter collagen fibres and reduced cartilage matrix.

缺乏c-Fos软骨细胞增殖较少，胶原纤维较短，且软骨基质减少。

We demonstrate that c-Fos controls chondrocyte response to microenvironmental stress caused by biomechanical and inflammatory cues.

们证明c-Fos控制软骨细胞对由生物力学和炎症信号引起微环境压力反应。

Eventually though, over the course of years, chondrocytes aren't able to keep up, and they become exhausted, and can undergo apoptosis, or programmed cell death.

最终，随着时间推移，软骨细胞力不从心，开始凋亡或程序性细胞死亡。

Importantly, ectopic expression of c-Fos in H2-c-fosLTR transgenic mice drives osteoblast and chondrocyte proliferation resulting in osteosarcoma and chondrogenic sarcoma.

重要是，H2-c-fosLTR转基因小鼠中c-Fos异位表达驱动了成骨细胞和软骨细胞增殖，导致了成骨肉瘤和软骨肉瘤形成。

For example, c-Jun is required for joint cell specification and intervertebral disc formation, while Fra2 regulates cartilage development and chondrocyte differentiation.

例如，c-Jun 对关节细胞特化和椎间盘形成是必需，而 Fra2 调节软骨发育和软骨细胞分化。

In healthy people, chondrocytes maintain a delicate balance between breaking down old cartilage—called catabolic activity, and producing new cartilage—called anabolic activity, through the use of both degradative enzymes and synthetic enzymes.

在健康机体内，软骨细胞在分解老化软骨（分解作用）和产生新软骨（合成作用）之间通过分解酶和合成酶来保持精细平衡。

This implies that chondrocytes maintain the structural and functional integrity of cartilage and sense microenvironmental changes during OA onset, although the underlying cartilage protective mechanisms remain elusive.

这表明，在骨关节炎初期，软骨细胞维持着软骨结构和功能完整性，并能感知微环境变化，尽管潜在软骨保护机制仍然不明。

Importantly, mutations in cartilage matrix genes such as COL2A1, COL9A3, COL11A2 and cartilage oligomeric matrix protein (COMP), which are produced by articular chondrocytes, cause chondrodysplasia with early-onset OA.

重要是，软骨基质基因如COL2A1、COL9A3、COL11A2和软骨寡聚基质蛋白（COMP）突变，这些基因由关节软骨细胞产生，导致软骨发育不良并伴早期发病骨关节炎。

One gene in particular involved in regulating cilia was missing a small piece found in all other birds and mammals Cilia on cells called chondrocytes pass on important signals during development.

一个特别参与调节纤毛基因缺失了一小段，在所有其他鸟类和哺乳动物中发现了这一点。纤毛在称为软骨细胞细胞上，在发育过程中传递重要信号。

The concern here is that if you apply a heavy external force, like lifting weights, onto these epiphyseal 'growth' plates, you damage the chance for your chondrocytes cells to grow, cutting potential height growth.

这里问题是，如果你在这些骨骺生长板上施加一个沉重外力，比如举重，你就破坏软骨细胞生长机，阻断了可能生长高度。

How articular chondrocytes, that primarily rely on glycolysis in low oxygen homoeostatic conditions, respond to joint damage and adapt to microenvironmental changes in articular cartilage is an important yet poorly understood question.

关节软骨细胞主要依赖于低氧稳态条件下糖酵解，它们如何响应关节损伤并适应关节软骨微环境变化，是一个非常重要但尚不完全理解问题。

MSCs differentiate into adipocytes, osteocytes, chondrocytes, tenocytes, marrow stromal cells, muscle, and perhaps neuronal cells and are being used in early clinical trials to enhance bone marrow grafting and to suppress graft-versus-host disease in allogeneic bone marrow transplants.

MSCs分化成脂肪细胞，骨细胞，软骨细胞，肌腱细胞，骨髓基质细胞，肌肉和神经细胞，并用于早期临床试验，以增强骨髓移植和抑制同种异体骨髓移植中移植物抗宿主病。