In a significant stride forward in cardiovascular research, scientists at the University of Aberdeen have reported promising results in the fight against heart disease with a drug named Trodusquemine.
Building on their groundbreaking 2017 research, the team has now demonstrated that this drug can effectively “block” fat accumulation in arteries in animal models and human cells.
The original study conducted at the Aberdeen Cardiovascular and Diabetes Center revealed that Trodusquemine could reverse fat build-up inside the arteries of mice.
This fat build-up, known as aortic plaque, is a key factor in the development of atherosclerosis, a major cause of heart attacks and strokes.
The drug worked by inhibiting an enzyme called PTP1B, which is known to contribute to this harmful process.
The latest research, published in the Journal of Translational Medicine, took this investigation a step further by testing Trodusquemine on white blood cells from humans.
The study included 30 healthy volunteers and 30 individuals with coronary artery disease and atherosclerosis. The researchers observed that the drug induced the same biochemical changes in human cells as seen in mice.
This finding is significant as it suggests the potential for Trodusquemine to be used in treating heart disease in humans.
PTP1B plays a pivotal role in the body’s response to obesity, diabetes, and certain inflammatory conditions. When PTP1B levels are high, it triggers a cascade of events leading to white blood cells absorbing oxidized cholesterol.
These cells then transform into “foam cells,” contributing to the fatty deposits in arteries and escalating inflammation.
Trodusquemine’s mechanism of action appears to be blocking the effects of this immune response, preventing the formation of these harmful foam cells.
This could be key in preventing the accumulation of fatty deposits in arteries, a major contributor to heart disease.
Furthermore, the research indicated that genetically removing PTP1B in mice resulted in lower cholesterol levels, particularly the “bad” LDL cholesterol, and improved cell communication, which is often impaired in heart disease.
Professor Mirela Delibegovic, who led the study, expressed optimism about these findings, stating that they complement their previous work and show the potential of Trodusquemine as a novel therapeutic approach to combat atherosclerosis.
The success in preclinical models and now in human cells has paved the way for potential clinical trials.
Professor James Leiper of the British Heart Foundation also acknowledged the significance of these results. He emphasized the importance of further research to confirm the efficacy of PTP1B inhibition in human subjects.
This study marks an important advance in understanding and potentially treating heart disease.
By demonstrating the effectiveness of Trodusquemine in blocking harmful processes in the arteries, it offers hope for new, more effective treatments for atherosclerosis and related cardiovascular conditions.
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The research findings can be found in the Journal of Translational Medicine.
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