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The transcriptomic and epigenetic landscapes of developing human articular and growth plate cartilage reveal putative gene regulatory networks governing lineage commitment and tissue homeostasis.

NFATc1 is identified as a molecular marker of articular cartilage progenitor cells and a transcriptional repressor of chondrocyte differentiation, providing fundamental insights into the origin and differentiation mechanism of articular chondrocytes.

Meniscal Gli1+ cells are mesenchymal progenitors that contribute to the development and injury repair of meniscus.

Bioinformatic analysis of mesenchymal stem cell chondrogenesis identified a novel long noncoding RNA, GRASLND, which suppresses interferon signaling and enhances chondrogenesis.

A multi-disciplined approach uncovered microRNA-199a/b-5p as important regulators of chondrogenesis, which negatively regulate mRNAs such as FZD6, ITGA3, and CAV1 for protective purposes during chondrogenesis.

A long non-coding RNA called GRASLND is essential to help stem cells create stable cartilage.

The ability of cartilaginous fishes to generate new cartilage through adulthood, and to spontaneously repair damaged cartilage, could shed light on novel cell-based therapies for cartilage injury in mammals.

Zebrafish have lubricated joints similar to ours and are a tractable model for arthritis research.

Using genetics, it is possible to uncouple higher adiposity from its adverse metabolic effects and show that some obesity-associated conditions may benefit from treating the metabolic effects alone, whilst others may benefit more from weight loss.

Glutamine deprivation reprograms chondrocytes, attenuates inflammation, and such intervention may be protective against joint inflammation.