A5034281435- Protein Degradation and Inhibitors
- Autophagy in Disease and Therapy
- Cardiac Fibrosis and Remodeling
- Peptidase Inhibition and Analysis
- Signaling Pathways in Disease
- Genetics and Neurodevelopmental Disorders
- Advancements in Semiconductor Devices and Circuit Design
- Cardiomyopathy and Myosin Studies
- Epigenetics and DNA Methylation
- Tissue Engineering and Regenerative Medicine
- Receptor Mechanisms and Signaling
- Histone Deacetylase Inhibitors Research
- Pulmonary Hypertension Research and Treatments
- Studies on Chitinases and Chitosanases
- Genetics, Aging, and Longevity in Model Organisms
- Cardiovascular Function and Risk Factors
- Renal and related cancers
- Cardiac tumors and thrombi
- Cardiac Ischemia and Reperfusion
- Congenital heart defects research
- Muscle Physiology and Disorders
- Hormonal Regulation and Hypertension
- Pancreatic function and diabetes
QIMR Berghofer Medical Research Institute
2020-2025
Queensland University of Technology
2025
Bioengineering Center
2023
Radboud University Nijmegen
2020-2021
Radboud University Medical Center
2020-2021
Crosstalk between cardiac cells is critical for heart performance. Here we show that vascular within human organoids (hCOs) enhance their maturation, force of contraction, and utility in disease modeling. Herein optimize our protocol to generate populations addition epicardial, fibroblast, cardiomyocyte self-organize into in-vivo-like structures hCOs. We identify mechanisms communication endothelial cells, pericytes, fibroblasts, cardiomyocytes ultimately contribute organoid maturation. In...
Macroautophagy (hereafter referred to as autophagy) is a finely tuned process of programmed degradation and recycling proteins cellular components, which crucial in neuronal function synaptic integrity. Mounting evidence implicates chromatin remodeling fine-tuning autophagy pathways. However, this epigenetic regulation poorly understood neurons. Here, we investigate the role KANSL1, member nonspecific lethal complex, acetylates histone H4 on lysine 16 (H4K16ac) facilitate transcriptional...
Cardiomyocytes (CMs) lost during ischemic cardiac injury cannot be replaced due to their limited proliferative capacity. Calcium is an important signal transducer that regulates key cellular processes, but its role in regulating CM proliferation incompletely understood. Here we show a robust pathway for new calcium signaling-based regenerative strategies. A drug screen targeting proteins involved cycling human embryonic stem cell-derived organoids (hCOs) revealed only the inhibition of...
Abstract Autophagy is a finely tuned process of programmed degradation and recycling proteins cellular components, which crucial in neuronal function synaptic integrity. Mounting evidence implicates chromatin remodelling fine-tuning autophagy pathways. However, this epigenetic regulation poorly understood neurons. Here, we investigate the role KANSL1, member nonspecific lethal complex, acetylates histone H4 on lysine 16 (H4K16ac) to facilitate transcriptional activation. Loss-of-function...
Abstract Induction of cardiomyocyte proliferation to replace damaged heart tissue is a promising therapeutic approach. A recent drug screen revealed that cardiomyocytes require the mevalonate pathway for proliferation, although specific mechanisms are unknown. In this study, we use human pluripotent stem cell-derived and cardiac organoids further interrogate role in proliferation. Chemical genetic perturbations indicated post-translational modification, prenylation, regulates We prenyl...
SUMMARY Cardiac injury and dysfunction occur in COVID-19 patients increase the risk of mortality. Causes are ill defined, but could be direct cardiac infection and/or inflammation-induced dysfunction. To identify mechanisms cardio-protective drugs, we use a state-of-the-art pipeline combining human organoids with phosphoproteomics single nuclei RNA sequencing. We an inflammatory ‘cytokine-storm’, cocktail interferon gamma, interleukin 1β poly(I:C), induced diastolic Bromodomain-containing...
Background: Cardiomyocytes (CMs) lost during ischemic cardiac injury cannot be replaced due to their limited proliferative capacity, which leads progressive heart failure. We and others have shown that reduced CM contractility can promote cell cycle induction; however, the underlying mechanisms are still unclear. Calcium (Ca 2+ ), a key regulator of contractility, is also an important signal transducer regulates cellular processes. Ca enters CMs through LTCC, triggers release from...
Abstract Cardiomyocytes (CMs) lost during ischemic cardiac injury cannot be replaced due to their limited proliferative capacity, which leads progressive heart failure. Calcium (Ca2+) is an important signal transducer that regulates key cellular processes, but its role in regulating CM proliferation incompletely understood. A drug screen targeting proteins involved calcium cycling human embryonic stem cell-derived organoids (hCOs) revealed only the inhibition of L-Type Channel (LTCC), not...
Cardiac injury and dysfunction occur in COVID-19 patients increase the risk of mortality. Causes are ill defined, but could be direct cardiac infection and/or 'cytokine-storm' induced dysfunction. To identify mechanisms discover cardio-protective drugs, we use a state-of-the-art pipeline combining human organoids with high throughput phosphoproteomics single nuclei RNA sequencing. We that diastolic can caused by cocktail interferon gamma, interleukin 1β poly(I:C) also serum. Bromodomain...