A5076449758- Mitochondrial Function and Pathology
- Cardiac Ischemia and Reperfusion
- ATP Synthase and ATPases Research
- Lipoproteins and Cardiovascular Health
- Atherosclerosis and Cardiovascular Diseases
- Coffee research and impacts
- Cardiac Fibrosis and Remodeling
- Anesthesia and Neurotoxicity Research
- Autophagy in Disease and Therapy
- Diabetes, Cardiovascular Risks, and Lipoproteins
- Genetics and Physical Performance
- Extracellular vesicles in disease
- Cholesterol and Lipid Metabolism
- Cardiovascular Disease and Adiposity
- Coconut Research and Applications
- Adipokines, Inflammation, and Metabolic Diseases
- High Altitude and Hypoxia
- Cell Adhesion Molecules Research
- Cardiovascular Function and Risk Factors
- Nitric Oxide and Endothelin Effects
- Connexins and lens biology
- GDF15 and Related Biomarkers
- Circular RNAs in diseases
- Signaling Pathways in Disease
- Phagocytosis and Immune Regulation
National Heart Centre Singapore
2018-2024
National University of Singapore
2018-2024
Justus-Liebig-Universität Gießen
2019-2024
Duke-NUS Medical School
2018-2023
There remains an unmet need to identify novel therapeutic strategies capable of protecting the myocardium against detrimental effects acute ischemia-reperfusion injury (IRI), reduce myocardial infarct (MI) size and prevent onset heart failure (HF) following infarction (AMI). In this regard, perturbations in mitochondrial morphology with imbalance fusion fission can disrupt metabolism, calcium homeostasis, reactive oxygen species production, factors which are all known be critical...
Objective- Atherosclerotic coronary artery disease is the leading cause of death worldwide, and current treatment options are insufficient. Using systems-level network cluster analyses on a large case-control cohort, we previously identified PCSK3 (proprotein convertase subtilisin/kexin family member 3; FURIN) as several disease-associated pathways. Thus, our objective to determine role FURIN in atherosclerosis. Approach Results- In vitro, inhibitor resulted reduced monocyte migration...
Background: New treatments are needed to reduce myocardial infarct size (MI) and prevent heart failure (HF) following acute infarction (AMI), which the leading causes of death disability worldwide. Studies in rodent AMI models showed that genetic pharmacological inhibition mitochondrial fission, induced by ischemia reperfusion, reduced MI size. Whether targeting fission at onset reperfusion is also cardioprotective a clinically-relevant large animal model remains be determined. Methods:...
Abstract Aims Genetic and pharmacological inhibition of mitochondrial fission induced by acute myocardial ischaemia/reperfusion injury (IRI) has been shown to reduce infarct size. The clinically used anti-hypertensive heart failure medication, hydralazine, is known have anti-oxidant anti-apoptotic effects. Here, we investigated whether hydralazine confers cardioprotection inhibiting Drp1-mediated fission. Methods results Pre-treatment with was inhibit both membrane depolarisation oxidative...
Caffeine is among the most highly consumed substances worldwide, and it has been associated with decreased cardiovascular risk. Although caffeine shown to inhibit proliferation of vascular smooth muscle cells (VSMCs), mechanism underlying this effect unknown. Here, we demonstrated that VSMC induced macroautophagy/autophagy in an vivo injury model restenosis. Furthermore, studied effects primary human mouse aortic VSMCs immortalized VSMCs. cell proliferation, autophagy flux via inhibition...
Aims: Bats are unique mammals with remarkable adaptations, including powered flight, which demands significant energy expenditure. While previous studies have documented basic structural characteristics of bat hearts, a comprehensive understanding their response to physiological stress remains unexplored. This study investigates the cardiac adaptations cave nectar Eonycteris spelaea elucidate mechanisms underlying capabilities. Methods and Results: We performed RNA sequencing analyse gene...
Abstract Despite strong evidence supporting the cellular interplay between haemostasis and innate immunity, humoral connections blood coagulation behavior of inflammatory macrophages are not well understood. In this study, we investigated changes in gene expression selected cytokines chemokines their secretion profiles following thrombin stimulation murine macrophages. Thrombin promoted differentiation into an M1-like phenotype that was associated with classical pro-inflammatory markers. The...
New treatments are needed to prevent neointimal hyperplasia that contributes post-angioplasty and stent restenosis in patients with coronary artery disease (CAD) peripheral arterial (PAD). We investigated whether modulating mitochondrial function using division inhibitor-1 (Mdivi-1) could reduce post-vascular injury by metabolic reprogramming of macrophages from a pro-inflammatory anti-inflammatory phenotype.
Vascular restenosis remains a major problem in patients with coronary artery disease (CAD) and peripheral (PAD). Neointimal hyperplasia, defined by post-procedure proliferation migration of vascular smooth muscle cells (VSMCs) is key underlying pathology. Here we investigated the role Interleukin 11 (IL-11) mouse model injury-related plaque development. Apoe-/- mice were fed hyperlipidaemic diet subjected to carotid wire injury right carotid. Mice injected an anti-IL11 antibody (X203), IgG...
Abstract Mitochondrial dysfunction induced by acute cardiac ischemia–reperfusion (IR), may increase susceptibility to arrhythmias perturbing energetics, oxidative stress production and calcium homeostasis. Although changes in mitochondrial morphology are known impact on function, their role arrhythmogenesis is not known. To assess action potential duration (APD) cardiomyocytes from the Mitofusins-1/2 (Mfn1/Mfn2)-double-knockout (Mfn-DKO) compared wild-type (WT) mice,...
Abstract Background Acute myocardial infarction (AMI) and post-infarct heart failure (HF) are among the leading causes of death disability worldwide. As such, new treatments urgently needed to protect against detrimental effects acute ischemia/reperfusion injury (IRI), in order prevent onset HF improve clinical outcomes following AMI. Given that mitochondrial dysfunction is a key determinant IRI-induced cardiomyocyte AMI, we investigated ND-13, 13-amino acid peptide derived from pro-survival...
Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main source(s): Singapore Medical Research Council Background New treatments are needed to prevent post-angioplasty and stent restenosis in coronary artery disease (CAD) peripheral arterial (PAD) patients. Accumulated findings have shown that mitochondrial dysfunction is involved the pathophysiology mechanisms underlying several cardiovascular conditions, however, scenario vascular remodelling...