October 2, 2025Open Access

Both terminal misfolding and polymerisation contribute to disease-relevant phenotypic changes in cell models of α1-antitrypsin deficiency-associated liver disease

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Cell studies reveal that both terminal misfolding and polymerisation contribute to fibrosis in liver disease.
Proteomic analysis indicates that responses to the Z mutation resemble those seen in the null Hong Kong variant.
Findings emphasize a need for therapies targeting both misfolding and polymerisation in alpha-1-antitrypsin deficiency.
Changes in cellular metabolism from oxidative to glycolytic pathways are linked to misfolding-related fibrosis.

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Analysis shows the role of polymerisation and terminal misfolding in liver disease, suggesting therapeutic pathways.

Stylianou et al. (2025) studied this question.

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