Targeting STAT3 provides a potential therapeutic strategy for obstructive sleep apnea-related fibrotic heart disease mediated by TSP1.

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.

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.

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

Nanoscale changes to individual collagen fibrils drive lung fibrosis.

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.

CFTR modulators have potent innate anti-inflammatory properties that can be measured in clinic, both ex vivo and in vitro, which can be used to predict treatment efficacy.

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.

Lymphangiogenic therapy VEGFCc156s improved angiotensin-II-induced impairments in heart function via novel mechanisms, which include transcriptional responses to alleviate inflammation and cardiac fibrosis, and systemic responses to ameliorate hypertension.