David W. Greening

This study identifies mechanosensory pathways in monocytes exposed to pathological shear stress, revealing PKC and Piezo1 as key regulators of monocyte phenotype and function in calcific aortic valve disease.

The paper develops a human cardiac microtissue model to study ischemia-reperfusion injury and shows that nanovesicles improve cardiomyocyte survival and function through proteomic changes.

This paper develops a dual-omics workflow to map subcellular proteome and lipidome in mouse heart, revealing sex-dependent molecular differences and conserved subcellular lipid features.

This paper develops an adhesive silk hydrogel patch for localized and sustained delivery of stem cell-derived nanovesicles, showing anti-fibrotic effects in vitro and in a mouse model.

This study shows that impairing polymerase gamma activity in cardiomyocytes leads to mtDNA instability, activates the integrated stress response, and causes severe cardiomyopathy with hepatopathy in mice.

This paper shows DRP1 inhibition reduces doxorubicin-induced cardiotoxicity while maintaining its anticancer effects in multiple cancer models.

This paper develops a device-encapsulated MSC system for sustained secretome delivery to treat ischaemic heart injury, showing improved cardiac function and reduced remodelling in rats.

The paper identifies hallmark protein and lipid features of circulating extracellular vesicles in humans using multi-omics analysis and provides an open-source tool for further exploration.

This study identifies proteomic changes in midbody remnants (MBRs) from MDCK cells and H-Ras-transformed cells during EMT, revealing distinct protein profiles associated with mesenchymal and epithelial states.

This study shows that muscle-specific PolG dysfunction causes mitochondrial dysfunction and cachexia by activating the mtISR and altering the mitochondrial folate cycle.

This study uses single-cell multiomic analysis to identify transcriptional circuits driving non-ischemic cardiac fibrosis in mouse and human hearts, showing reversibility of fibrosis-related changes.

This study uses patient-derived cerebral organoids to identify molecular and cellular mechanisms of Schizophrenia, revealing altered neuronal programming factors and growth factors like BRN2 and PTN.

This paper reports a proteomic analysis of schizophrenia patient-derived cerebral organoids, identifying 43 up-regulated and 54 down-regulated proteins, including GWAS factors and neuronal development-related proteins.

This study shows that astrocytes from ASD patients induce repetitive behavior and impair memory when transplanted into healthy mice, suggesting a primary role for astrocytes in ASD.