Michael P. Morley

The paper identifies shared and distinct genetic architectures for cardiac structure and function using UK Biobank data, revealing common variants influencing multiple chambers and phenotypic variability.

This study shows that mechanical-nuclear signaling in alveolar fibroblasts influences lung regeneration by modulating transcriptional identity and epithelial repair after injury.

This study identifies pathogenic MYBPC3 missense variants in HCM patients and shows they disrupt protein interactions and alter proximity to thin-filament proteins.

This study uses human living myocardial slices to examine how sodium glucose co-transporter inhibitors affect myocardial work in hypertrophic cardiomyopathy under varying loading conditions.

This study shows that Z-AAT expression in AT2 cells causes stress responses and increases emphysema risk in AATD.

The paper creates a postnatal human lung developmental atlas to identify genes linked to chronic lung disease risk and shows COPD genetic risk is enriched in genes active during early postnatal endothelial development.

This study identifies differentially expressed lncRNAs in a mouse HCM model and prioritizes them using cross-species conservation and micropeptide coding potential.

This study shows that alveolar epithelial type I cells propagate mechanical signals that affect lung homeostasis and disease states through intercellular communication.

This study maps the temporal sequence of mouse lung regeneration after viral injury, identifying persistent injury-associated cell states and their role in alveolar niche repair.

The paper identifies an injury-induced tissue niche (iTCH) in the lung that coordinates regenerative and disease responses through mesenchymal plasticity and signaling pathways.

This study identifies 80 genetic loci and 61 effector genes associated with dilated cardiomyopathy through GWAS and integrates transcriptomic data to uncover biological pathways and cellular states involved in the disease.

This study identifies 194 epigenome-wide significant CpGs associated with dilated cardiomyopathy (DCM) and links them to cardiac gene expression and cardiovascular risk factors.

The paper generates gene expression data from iPSC-derived cardiomyocytes in a multiethnic cohort and makes the results publicly available.

The paper constructs a single-cell reference atlas for human and mouse lung tissues to improve cell type annotation and data integration.

The paper identifies widespread epigenomic changes in idiopathic dilated cardiomyopathy, showing a shift toward fetal-like enhancer states and providing a data resource for further study.

This study performs a large GWAS on dilated cardiomyopathy, identifying two new loci and confirming two existing ones, with potential therapeutic implications.

This paper identifies novel genetic loci for cardiac disorders by analyzing the morphological effects of genetic variants across the entire cardiac cycle represented by the ECG.

This study conducts a large GWAS on heart failure, identifying 12 genetic loci with associations to CAD, atrial fibrillation, and reduced left ventricular function, and provides causal evidence for several risk factors.

The paper identifies genetic variants associated with heart failure by analyzing histone acetylation QTLs in human heart tissue.

The paper identifies PPP1R3A as a central cardioprotective factor in pressure overload heart failure by analyzing gene network rewiring in human hearts.