Author

A. Frustaci

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Pathology· 2

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Approach:experimental assay· 2 Research Focus:differential expression· 1 Research Focus:host-pathogen & immune response· 1 Organism:human· 1 Assay:imaging· 1 Organism:mouse· 1

Frequent Co-Authors

C. Chimenti· 2 shared M. A. Russo· 2 shared R. Verardo· 2 shared A. M. Shah· 1 shared A. Protti· 1 shared C. G. dos Remedios· 1 shared C. M. Shanahan· 1 shared D. Brayson· 1 shared

Activity by Year

2018-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 39 mutual co-author links

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2 shared papersPathology

C. Chimenti

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2 papers

Recent·Most cited

Fabry Cardiomyopathy: Myocardial Fibrosis, Inflammation and Down-Regulation of Mannose-6-Phosphate Receptors cause Low accessibility to Enzyme Replacement Therapy

A. Frustaci, R. Verardo, M. Magnocavallo, E. Frustaci, M. A. Russo, C. Chimenti

This study investigates the limited effectiveness of enzyme replacement therapy (ERT) in advanced Fabry disease cardiomyopathy, identifying myocardial fibrosis, inflammation, and reduced mannose-6-phosphate receptors as barriers to therapy.

bioRxiv · Dec 20, 2023Pathology

Accumulation of prelamin A drives inflammation in the heart with implications for treatment of inherited and acquired cardiomyopathies

D. Brayson, A. Frustaci, R. Verardo, C. Chimenti, M. A. Russo, R. Hayward, S. M. Ahmad, G. Vizcay-Barrena, A. Protti, P. S. Zammit, C. G. dos Remedios, E. Ehler, A. M. Shah, C. M. Shanahan

This study shows prelamin A accumulation drives inflammation in both inherited and acquired cardiomyopathies, suggesting potential treatment strategies targeting inflammation.

bioRxiv · Nov 28, 2018Pathology