Researchers at East Lansing’s MSU Invent Nanoparticle that Destroys Heart Attack-causing Plaque

Researchers at Michigan State University in East Lansing have partnered with Stanford University scientists to invent a nanoparticle that destroys portions of plaques that cause heart attacks. The discovery could be a treatment for atherosclerosis, a buildup of plaque in arteries and a leading cause of death in the U.S.
1355
nanoparticles in heart attack-causing plaque
MSU researchers have helped create nanoparticles (green) that enter heart attack-causing plaque and stimulates macrophages (red) to eat it away. // Image courtesy of Michigan State University

Researchers at Michigan State University in East Lansing have partnered with Stanford University scientists to invent a nanoparticle that destroys portions of plaques that cause heart attacks. The discovery could be a treatment for atherosclerosis, a buildup of plaque in arteries and a leading cause of death in the U.S.

The nanoparticle, created by Bryan Smith, associate professor of biomedical engineering at MSU, and a team of scientists, can be directed to eat debris, reducing and stabilizing plaque. It finds the plaque due to its high selectivity to monocytes and macrophages, a particular immune cell type found in the plaque. Once inside the macrophages in the plaques, the nanoparticle delivers a drug agent that stimulates the cell to engulf and eat cellular debris, removing the diseased and dead cells in the plaque core.

Smith expects future clinical trials will show a reduced risk of most types of heart attacks with minimal side effects due to the unprecedented selectivity of the nanodrug.

The team’s studies focus on interpreting the signaling of the receptors in the macrophages and sending a message via small molecules using nano-immunotherapeutic platforms. Previous studies have acted on the surface of cells, but this approach works intercellularly and has been effective in stimulating macrophages.

“We found we could stimulate the macrophages to selectively eat dead and dying cells – these inflammatory cells are precursor cells to atherosclerosis – that are part of the cause of heart attacks,” Smith says. “We could deliver a small molecule inside the macrophages to tell them to begin eating again.”

The approach is also expected to be usable in other applications.

“We were able to marry a groundbreaking finding in atherosclerosis by our collaborators with the state-of-the-art selectivity and delivery capabilities of our advanced nanomaterial platform,” Smith says. “We demonstrated the nanomaterials were able to selectively seek out and deliver a message to the very cells needed. It gives a particular energy to our future work, which will include clinical translation of these nanomaterials using large animal models and human tissue tests. We believe it is better than previous methods.”

Smith has filed a provisional patent and expects to begin marketing the nanoparticle later this year. The results were published in an article titled “Pro-efferocytic nanoparticles are specifically taken up by lesional macrophages and prevent atherosclerosis” in Nature Nanotechnology.