Parthenolide, Ero1L and MAM stabilization in localized scleroderma: abstract findings
In an abstract, parthenolide reduced senescence and fibrosis in TGF-β-treated human dermal fibroblasts and a mouse localized scleroderma model; the effect was mediated through Ero1L suppression and MAM stabilization. [1]
Automatic summary · not editorially reviewed
The key findings
In localized scleroderma skin lesions, MAM quantity increased and calcium ion transport function was enhanced. [1]
Parthenolide's protective effect was reported to be mediated through Ero1L suppression, and Ero1L overexpression reversed it. [1]
The PTL-loaded hydrogel showed sustained release and therapeutic efficacy in the mouse LoS model. [1]
The source at a glance
- Study type / format
- Preclinical laboratory and animal study (abstract)
- Population / context
- Human dermal fibroblasts treated with TGF-β and a bleomycin-induced mouse model of localized scleroderma; LoS skin lesions examined by electron microscopy.
- Summary based on
- Study abstract
- Original publication
- October 1, 2026
MAM changes in localized scleroderma skin lesions
The abstract reports that mitochondria-associated endoplasmic reticulum membranes (MAM) were examined in skin lesions of localized scleroderma (LoS) using transmission electron microscopy. MAM quantity increased, and its calcium ion transport function was enhanced. The authors state that mitochondrial dysfunction drives scleroderma pathogenesis and that MAM regulates mitochondrial function. These are observations from the abstract; the full text was not reviewed.
Supporting source [1]
Parthenolide effects in fibroblasts and a mouse LoS model
Parthenolide (PTL) ameliorated senescence and fibrosis in TGF-β-induced human dermal fibroblasts and in a bleomycin-induced mouse LoS model, according to the abstract. The authors link this to regulation of the IP3R1/Grp75/VDAC1 complex and repair of mitochondrial damage. Mechanistically, they report the protective effect was mediated through Ero1L suppression, with ARG-449 identified as the critical residue for PTL–Ero1L binding. Ero1L overexpression reversed the protective effects, and Ero1L knockdown also showed anti-senescence and antifibrotic effects in TGF-β-induced fibroblasts.
Supporting source [1]
Hydrogel delivery tested only in the mouse model
The abstract describes a synthesized thermosensitive controlled-release hydrogel, F127@PLGA@PTL, prepared with emulsification-volatilization. It is reported to show sustained-release properties and significant therapeutic efficacy in the mouse LoS model. The abstract concludes that PTL alleviates LoS fibrosis by regulating Ero1L-mediated MAM stabilization. These are preclinical cell and animal findings from an abstract; they do not establish benefit in people with LoS, and the full text was not reviewed.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings come from cell experiments and a mouse model, so human benefit is not established.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Wang F, Xing R, Xie M, Qin Y, Zhang Y, Cao D, He G, Lyu X. · europepmc.org · October 1, 2026