Author

Mathuscha Ratnasingham

University of Leicester

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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Cell Biology· 2

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:human· 2 Assay:proteomics· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1

Frequent Co-Authors

Catherine McMullan· 2 shared Katy Morgan RoachiD· 2 shared Molly Whitfield· 2 shared Peter H. BraddingiD· 2 shared Alfie J Hall· 1 shared Anita Valand· 1 shared Anvesha SinghiD· 1 shared Beatriz Goncalves· 1 shared

Activity by Year

2026-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 40 mutual co-author links

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2 shared papersCell Biology

Catherine McMullan

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Loss of PKN2 drives fibroblast reprogramming and extracellular matrix remodelling in pulmonary fibrosis

Catherine McMullan, Oscar A Peña, Poojitha Rajasekar, Anita Valand, Panayiota Stylianou, Gill Elliott, Molly Whitfield, Mathuscha Ratnasingham, Sahana Narayan, Alfie J Hall, Beatriz Goncalves, Vijay Mistry, Liesl Carr, Hilary Marshall, Bin Liu, , Katy Morgan Roach

This study shows that loss of PKN2 leads to fibroblast reprogramming and ECM remodelling in pulmonary fibrosis by altering key pathways and secretion.

bioRxiv · Sep 3, 2026 · PreprintCell Biology

KCa3.1 Drives Pro-Fibrotic Activation and Represents a Novel Therapeutic Target in Aortic Stenosis

Molly Whitfield, Saadia Aslam, João Goncalves De Sousa, Daniel Taveira, Catherine McMullan, Mathuscha Ratnasingham, Gill Elliiott, S M Duffy, Neil Craig, Stefan Alexander Veizades, Stephanie Sellers, Hiwa Sherzad, Metesh Acharya, Giovanni Mariscalco, Gerry Patrick McCann, , Katy Morgan Roach

This study shows KCa3.1 channels drive fibrosis in aortic stenosis by promoting myofibroblast contraction and collagen production, and inhibition with senicapoc reduces these effects.

bioRxiv · May 4, 2026 · PreprintCell Biology