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

因此软骨细对关节软骨非常重要。

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

所以你骨骼中的骨细就变了一个骨细。——软骨母细软骨细也是如此。

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

软骨肉瘤起源于软骨细，即产生软骨的细。

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的起始因素是什么，都会有软骨细开始尝试修复软骨。

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的加骨骼的长度，们称之软骨细。

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

保持关节软骨的健康是软骨细的工作；软骨细是负责一切软骨相关事务的特殊细。

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，人类和小鼠的OA软骨中FOS阳性的软骨细多。

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

缺乏c-Fos的软骨细较少，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控制软骨细对由生物力学和炎症信号引起的微环境压力的反应。

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，软骨细力不从心，开始凋亡或程序性细死亡。

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

重要的是，H2-c-fosLTR转基因小鼠中c-Fos的异位表达驱动了骨细和软骨细的，导致了骨肉瘤和软骨肉瘤的形。

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 对关节细的特化和椎间盘的形是必需的，而 Fra2 调节软骨的发育和软骨细的分化。

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.

在健康的机体内，软骨细在分解老化的软骨（分解作用）和产生新的软骨（合作用）之间通过分解酶和合酶来保持精细平衡。

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，软骨细维持着软骨的结构和功能完整性，并能感知微环境的变化，尽管潜在的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.

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

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的基因缺失了一小段，在所有其他鸟类和哺乳动物中都发现了这一点。纤毛在称软骨细的细上，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.

这里的问题是，如果你在这些骨骺生长板上施加一个沉重的外力，比如举重，你就会破坏软骨细生长的机会，阻断了可能生长的高度。

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.

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

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分化脂肪细，骨细，软骨细，肌腱细，骨髓基质细，肌肉和神经细，并用于早期临床试验，以强骨髓移植和抑制同种异体骨髓移植中的移植物抗宿主病。