Author

Alessio Lampis

Centre National de la Recherche ScientifiqueORCID 0009-0006-3909-1386Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Pathology· 2

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1 Assay:protein structure· 1

Frequent Co-Authors

Christophe SiraciD· 2 shared Émilie PinaultiD· 2 shared Gemma Martinez-RivasiD· 2 shared Karolina Weronika ŚwiderskaiD· 2 shared Sébastien BenderiD· 2 shared Alexa Rinsant· 1 shared Alexander CarpinteiroiD· 1 shared Amélie BonaudiD· 1 shared

Activity by Year

2025-2025 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 41 mutual co-author links

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2 shared papersPathology

Christophe SiracORCID

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2 papers

Recent·Most cited

PathologybioRxivPreprintDec 23, 2025

Accelerated Apolipoprotein A-II senile amyloidosis in a PAI-1 (plasminogen activator inhibitor 1) knock-out model

Gilles Roussine Codo, Pauline Duchatelet, Gemma Martinez-Rivas…·Christophe Sirac

This study shows PAI-1 knockout mice develop systemic AApoA-II amyloidosis at intermediate age, with amyloid deposits in multiple organs and urinary albumin as a biomarker, highlighting potential risks of PAI-1 inhibition in amyloidosis.

DOI 10.64898/2025.12.18.695159

mouseexperimental assay

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PathologyNature CommunicationsPeer-reviewedMar 27, 2025

A mouse model of cardiac AL amyloidosis unveils mechanisms of tissue accumulation and toxicity of amyloid fibrils

Gemma Martinez-Rivas, Maria Victoria Ayala, Sébastien Bender…·Christophe Sirac

This paper develops a mouse model of cardiac AL amyloidosis that reproduces human disease features, including amyloid deposits and cardiac dysfunction, and identifies a role for partial LC degradation in fibril formation.

14 citationstop 1%

mouseprotein structure

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