Hydroxychloroquine induces autophagic cell death of human dermal fibroblasts: implications for treating fibrotic skin diseases.
Hydroxychloroquine (HCQ) is widely used to treat rheumatic and inflammatory diseases. It inhibits inflammation by downregulating the effects of inflammatory cells and their mediators. Although HCQ has been used to treat several fibrotic skin diseases, the mechanisms by which it exerts its effects on human dermal fibroblasts (HDFs) have not been studied in detail. In this issue, Ramser et al. show that HCQ inhibits proliferation of HDFs and induces autophagy. These observations are supported by the demonstration that HCQ upregulates Beclin-1, a key regulator of autophagy. Future studies are needed to determine whether HCQ induces autophagy in vivo and whether antimalarials have antifibrotic effects when used in clinically relevant doses.
Oikarinen
Aarne
A
Department of Dermatology, University of Oulu and Oulu University Hospital, Oulu, Finland. aarne.oikarinen@oulu.fi
D000962:Antimalarials / Q000494:pharmacology / Q000627:therapeutic use; D001343:Autophagy / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects; D020405:Dermis / Q000187:drug effects / Q000473:pathology*; D004305:Dose-Response Relationship, Drug; D005347:Fibroblasts / Q000187:drug effects / Q000473:pathology*; D005355:Fibrosis; D006801:Humans; D006886:Hydroxychloroquine / Q000494:pharmacology* / Q000627:therapeutic use*; D012871:Skin Diseases / Q000188:drug therapy* / Q000473:pathology
D000962:Antimalarials; D006886:Hydroxychloroquine