Author

Yiangos Psaras

British Heart FoundationORCID 0000-0002-8697-6121Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Signature Assays, Organisms & Methods

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Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Approach:experimental assay· 1 Approach:genetic perturbation / CRISPR· 1 Organism:mouse· 1

Frequent Co-Authors

Christopher N. ToepferiD· 2 shared Adam Linekar· 1 shared Alexander J. SparrowiD· 1 shared Andreas KoschinskiiD· 1 shared Betty RamaniD· 1 shared Charlotte L. Hooper· 1 shared Connor M. BlairiD· 1 shared Craig A. LygateiD· 1 shared

Activity by Year

2025-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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2 shared papersCell Biology

Christopher N. ToepferORCID

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2 papers

Recent·Most cited

Unmasking Supervillin: SVIL haploinsufficiency causes hypertrophic cardiomyopathy by impairing mechanotransduction and cellular energetics.

Yifan Joshua Li, Yiangos Psaras, Violetta Steeples, Josephine M Watkins, Charlotte L. Hooper, Marta Moya‐Jódar, T. NICOL, Alexander J. Sparrow, Marcos Garcia-Lacarte, S H Jones, Isabelle Bond, Niklas Beyhoff, Paul Robinson, Marieluise Kirchner, Philipp Mertins, , Christopher N. Toepfer

This study identifies SVIL haploinsufficiency as a cause of hypertrophic cardiomyopathy by impairing mechanotransduction and cellular energetics, with potential therapeutic implications for mitochondrial-targeted treatments.

bioRxiv · Jul 24, 2026 · PreprintCell Biology

Precision Targeting of Troponin I Phosphorylation Prevents Diastolic Dysfunction while Preserving Systolic Performance

Ying‐Chi Chao, Debra J. McAndrew, David Revuelta, Rahul Yadav, Wan-Hua Hong, Jianshu Hu, Milda Folkmanaite, Edoardo Valli, Mariana Gee Olmedilla, Andreas Koschinski, Nicoletta Concetta Surdo, Jakub Tomek, Diederik W.D. Kuster, Helen V. Edwards, Connor M. Blair, , Manuela Zaccolo

This paper identifies a nanodomain mechanism regulating troponin I phosphorylation and demonstrates a peptide that selectively enhances relaxation without compromising systolic function in heart failure.

bioRxiv · Nov 18, 2025 · PreprintCell Biology