Listen & Subscribe

Get The Latest FutureTech Podcast News Delivered Right To Your Inbox

Dr. Akbar is interested in how our body’s over-response can cause protective inflammation in heart disease and strokes that does more harm in our metabolic systems. His extracellular vesicles research may hold the key to these signals. He describes:

  • Exactly how immunological responses to heart attacks cause inflammation that is ultimately harmful.
  • Why atherosclerosis plaque buildup leads to an immune response that causes a cascade that leads to even more fat cell buildup.
  • Why extracellular vesicles research into exact signals sent through the spleen may hold the key to adjusting these signals therapeutically.

Dr. Naveed Akbar focuses on extracellular vesicles research and metabolic disease. Atherosclerosis, a long-term condition that often leads to heart attacks and strokes through ruptures, exemplifies how our immune system and metabolic system have a helpful and harmful relationship. The connection between diabetics and worse manifestations of atherosclerosis holds an important clue to the signals that may be in play. 

Atherosclerosis is a gradual condition that takes years to take hold and exists in a wide population. But what’s unclear is why diabetic patients have thicker and fattier plaques. Dr. Akbar believes this is because they have an immunological disease as well.

This led to a stronger focus on immune system response to these conditions. Ultimately the various over-responses of the immune system increases the plaque layers and inflammation. Dr. Akbar discusses how his research attempts to engage or disengage these responses in appropriate ways.

He especially is focused on extracellular vesicles research post metabolic disease. He’s found that immune cells travel to the heart and increase harmful inflammation. But by researching what signals cause this and how these signals can be manipulated, there’s hope for therapeutic responses.

For more information, see his page on the Oxford University site:

Accessibility Close Menu
Accessibility menu Accessibility menu Accessibility menu
× Accessibility Menu CTRL+U