Research
What is cardiometabolic disease?
Cardiometabolic disease (CMD) describes a group of illnesses that, together, are the number one cause of death worldwide. CMDs include obesity, heart disease, high blood pressure, diabetes, kidney disease, and unhealthy cholesterol levels. CMDs are are mainly caused by an unhealthy lifestyle, particularly smoking, lack of exercise, and/or an unhealthy diet; but a person's genetics can also directly impact disease severity.
Aren't mitochondria just "the powerhouse of the cell"?
While mitochondria are indeed responsible for generating almost all of our cells' energy, they are also responsible for many other functions including calcium homeostasis, generating body heat and signalling molecules, coordinating the recycling of damaged cells, initiating cell death, sensing changes in environmental oxygen, and mediating cell division. Mitochondria also have their own DNA - a smaller genome, passed on to all offspring by mothers only, that contains a record of prehistoric human migration out of Africa.
Why study mitochondria and CMDs?
While CMDs have reached epidemic levels around the world, some people are more sick than others, even after controlling for age, sex, socioeconomic status, access to healthcare, etc. and the pattern of this differential disease susceptibility matches that of mitochondrial genetic ancestry. This genetic link, coupled with the links between energy production and the mitochondria, make these organelles a likely key player in the pathogenesis of CMDs.
Mitochondria are master regulators of cellular metabolism, yet the mechanisms linking mitochondrial function to differences in cardiometabolic disease (CMD) risk and prognosis remain unclear. At MitoMetabLab, we investigate the interplay between mitochondrial genetics, mitochondrial dynamics (shape, structure, and network organization), mitochondrial bioenergetics, and metabolomics, large-scale profiling of metabolites that reflect nutrient use. We also study the signalling pathways that regulate inflammation, vascular function, and cell proliferation.
Using preclinical models and human participants with diverse mitochondrial genetic ancestry, we aim to define how mitochondrial DNA variation and metabolic rewiring shape disease outcomes. We are also developing platelet-based assays to provide a minimally invasive “mitochondrial-metabolomic fingerprint” for CMDs that can be deployed in the clinic.
Our goals are to: i) improve early detection of high-risk individuals; ii) identify new therapeutic targets; and iii) integrate mitochondrial biology into precision medicine to reduce the global burden of CMD.
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