Richard J. Mills

This paper develops PT-enhanced kidney organoids with S3-like cells to model physiological responses in CKD, showing improved functionality and scalability.

This study shows that gene therapy with AAV-ALPK3 improves heart function in mouse and human models of cardiomyopathy caused by ALPK3 variants.

The paper identifies a compound that selectively promotes cardiomyocyte proliferation through specific cell cycle mechanisms without affecting other cell types.

This study uses iPSC-derived muscle models to show that DUX4 base editing improves muscle function in childhood-onset FSHD.

This study shows that ageing reduces the phospho-proteomic response to resistance exercise in human skeletal muscle, despite normal mTORC1 activation, suggesting new therapeutic targets for aged muscle.

This paper benchmarks spatial transcriptomics in stem cell-derived organoids using Stereo-seq, optimizing RNA capture and introducing regional analysis methods.

This study identifies prenylation as a regulator of cardiomyocyte proliferation through multiple targets, suggesting its potential for cardiac regeneration.

This study identifies glycophagy dysregulation as a mechanism of diabetic heart disease and shows that Gabarapl1 gene therapy improves cardiac function in diabetic mice and human cardiac organoids.

The paper shows that inhibiting contractile function in cardiomyocytes reactivates the cell cycle, suggesting active contraction maintains differentiation and cell cycle arrest.

This study shows that maturing human cardiac organoids enhances disease modeling and drug discovery by mimicking in vivo development and enabling therapeutic testing for DSP cardiomyopathy.

The paper identifies UFMylation as a negative regulator of skeletal muscle function through proteome-wide systems genetics in mice and validates it in a disease model.

This study identifies HOPX as a molecular switch regulating cardiomyocyte progenitor and maturation gene programs, linking it to cardiac function and genetic variation.

This study identifies Gabarapl1 as a regulator of glycophagy in diabetic cardiomyopathy, showing its role in preventing glycogen accumulation and diastolic dysfunction.