PDGFRα+ Sca-1+ bone marrow stromal/stem cells in whole bone marrow grafts can trigger the onset of autoimmune-related fibrosis in a mouse model of scleroderma.

Telomerase gene therapy represents a novel effective treatment for pulmonary fibrosis associated with short telomeres by improving pulmonary function, decreasing inflammation and accelerating fiber disappearance in fibrotic lungs.

Nanoscale changes to individual collagen fibrils drive lung fibrosis.

Inhibition of S100a4 represents a novel anti-fibrotic target to improve tendon healing.

Aqueous solubility of cystic fibrosis drug ivacaftor is ~200-fold lower, whereas the potency of its stimulatory effect on the CFTR channel is >100-fold higher, than reported, and is fully reversible.

Dysfunction and overexpression of ENaC-mediated sodium influx exacerbates activation of NLRP3-inflammasome mediated inflammation in cells with CF-associated mutations and is modulated by inhibition of these amiloride-sensitive sodium (Na⁺) channels.

Fibro-inflammatory progenitors represent a subpopulation of perivascular cells in visceral adipose tissues of mice that promote inflammation and fibrosis.

Analysis of the mechanism of action of cystic fibrosis corrector drugs reveals signalling pathways potently controlling the proteostasis of the main disease-relevant CFTR mutant.

Tendon fibroblast cells lay down a collagen matrix template during embryogenesis, and the expansion of this matrix drives post-natal tissue growth.

The membrane type I-matrix metalloproteinase is essential for the release of collagen fibrils from plasma membrane fibripositors, which is required for the transition from embryonic to postnatal tendon development.