Loss of the CYLD tumour suppressor results in lung fibrosis in a mouse model, reports a study published in Nature Communications this week. These findings shed further light on the detailed mechanisms involved in lung fibrosis.
The CYLD tumour suppressor was originally identified as being mutated in cylindromatosis - a disease associated with multiple benign tumours of the skin. Jian-Dong Li and colleagues now report a role for this protein in the prevention of lung fibrosis in mice mediated by Streptococcus pneumoniae infection or the chemotherapeutic bleomycin. The authors previously showed that CYLD can prevent features associated with acute S.pneumoniae infection but now show that it blocks signalling pathways associated with the chronic disease, fibrosis. Mice lacking CYLD have enhanced fibrosis compared to wild-type mice after infection and samples of human lung fibrosis show reduced levels of CYLD.
These findings suggest that CYLD and the signalling pathways that it regulates could be key targets for designing new therapeutic strategies for preventing lung fibrosis.
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