In an endeavor that offers a glimmer of hope to individuals globally, an international team of scientists, which includes a specialist from the University of Virginia, has uncovered nearly a dozen genes that are linked to the calcium accumulation in our coronary arteries.
This build-up can pave the way for coronary artery disease, a formidable condition that accounts for up to one in four deaths in the United States.
Getting to the Heart of Calcium Build-up
Before people are diagnosed with atherosclerotic coronary artery disease, doctors can detect the early warning signs by spotting calcium buildup in the walls of coronary arteries.
They use non-invasive CT scans for this, as this calcium accrual is a solid predictor of forthcoming cardiovascular events, like heart attacks or strokes, and is also related to other age-related illnesses such as dementia and chronic kidney disease.
The focus of the research, published in Nature Genetics, was to delve deeper into our genetic makeup to identify factors that influence our susceptibility to this perilous calcium buildup.
Clint L. Miller, a researcher from the UVA School of Medicine, emphasized that discovering new genes related to clinical coronary artery disease is crucial.
This becomes a pivotal first step in pinpointing biological aspects to concentrate on for preventing the disease from developing in the first place.
Unraveling the Genetic Ties
Previously, the genetic aspect of coronary calcium buildup was somewhat recognized, yet only a few responsible genes were identified.
Thus, Miller and his team were determined to disclose new genetic variables that augment our risk for this calcium accumulation.
To achieve this, they analyzed data derived from over 35,000 individuals of European and African ancestry globally, in what stands as the largest “meta-analysis” conducted thus far to comprehend the genetic foundation of coronary artery calcification.
The diligent analysis of data enabled the scientists to pinpoint more than 40 prospective genes at 11 different chromosome locations tied to coronary artery calcification.
Among these, eight locations hadn’t been previously associated with coronary calcification, and five were new in relation to coronary artery disease.
Interestingly, one of the identified genes, ENPP1, is altered in uncommon forms of arterial calcification in infants.
From Discovery to Practical Application
The revelation of these genes’ involvement in coronary artery calcification has opened new avenues for scientists to work on developing drugs or repurposing existing ones, which can target these genes or the proteins they encode, to regulate the calcification process.
Some of these newly identified targets may even be influenced by dietary alterations or nutrient supplementation, such as vitamins C or D.
While further research is pivotal to ascertain the most effective ways to target these genes and affected pathways, Miller is optimistic that these discoveries could pave the way for enhanced patient risk evaluation or early interventions.
This means that the progression of coronary artery disease could potentially be halted before it fully manifests, representing a significant leap in treating a disease that globally accounts for over 17 million deaths annually.
“This interdisciplinary collaboration reveals the power of meta-analyses for an understudied and clinically relevant measurement,” Miller shared.
The findings have sown seeds of hope for continued progress in transitioning these preliminary findings into practical clinical applications and identifying additional genes that could extend risk prediction across more diverse populations.
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The research findings can be found in Nature Genetics.
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