Discovery of Heart Protein AIMP3 Highlights New Target for Cardiac Disease Treatments

Recent research conducted by molecular biologists at Brown University has identified a critical role for the protein AIMP3 in maintaining heart health. Published in Nature Cardiovascular Research, the study reveals that AIMP3 is essential for proper heart function and survival. The team used gene editing techniques to delete AIMP3 in mice, leading to severe cardiac issues such as inflammation, tissue scarring, and ultimately, heart failure.

Initially, AIMP3 was an unstudied protein with an unclear function within the heart. However, findings from the study demonstrate that AIMP3 is vital for preventing errors during protein synthesis in cardiac cells. It acts by supporting the editing activity of MetRS, a protein responsible for removing harmful substances like homocysteine. Without AIMP3, homocysteine accumulates, causing oxidative stress, protein aggregation, and mitochondrial defects, which lead to cell death.

The research team, led by postdoctoral researcher Anindhya S. Das, showed that deficiency of AIMP3 results in significant damage to heart cells and the development of severe cardiac diseases. They believe this protein has a broader role in other organs, given that it influences cellular health beyond the heart.

Understanding the mechanisms behind AIMP3’s protective effects opens new avenues for treating heart conditions associated with homocysteine buildup. Future studies aim to explore ways to boost AIMP3 levels or enhance its activity to prevent or treat heart disease. As cardiovascular disease remains the leading cause of death globally, this discovery marks an important step towards innovative therapeutic strategies.

Further details can be found in the original study here: Nature Cardiovascular Research.