Karen Piper Hanley

Karen Piper Hanley is Professor of Molecular Medicine and Head of Division in the Division of Diabetes, Endocrinology & Gastroenterology at the University of Manchester. She serves as the fibrosis lead in the Wellcome Trust Centre for Cell-Matrix Research and previously served as Director of Core Research Technologies (2019-2022). She is also an editorial board member for Scientific Reports.

Her research focuses on fibrosis (scarring) mechanisms across multiple organs, particularly liver, kidney, and lung fibrosis. Her lab investigates the cellular and molecular basis of fibrotic disease, with emphasis on how pathological scar components are produced and how they signal to surrounding cells. Key areas include the role of SOX9 transcription factor, integrin beta-1 signaling, Group 1 PAKs, and YAP1 in fibrosis progression.

Her recent publications reveal trends toward increased clinical translation of fibrosis research, with studies on health inequalities in liver cancer care, post-COVID diabetes incidence, and innovative approaches to liver disease detection. Her work increasingly integrates spatial transcriptomics and advanced omics technologies to understand cellular transitions in liver disease.

• Career-track postdoctoral fellowship from the University of Southampton (2006)

As senior postgraduate tutor, she has mentored numerous PhD students who have presented at key conferences and authored high-quality manuscripts. All her PhD students have submitted and been awarded their degrees within 4 years. She has successfully guided previous Academic Clinical Fellows to win MRC clinical training fellowships. Her teaching extends to undergraduate Personal & Professional Development and supervision of MRes and BSc students, many of whom have achieved first-class degrees and prestigious awards.

Her lab maintains active collaborations with Professor Neil Hanley's group on human development, stem cells, and regenerative medicine, bridging developmental biology with fibrosis research to understand why regeneration is impaired in chronic diseases.