Cardiovascular

Cell culture and mouse studies suggest Tregs or factors secreted by Tregs could help treat MI. In primary rat cardiomyocytes, supernatant derived from the media of primary rat Treg cultures increased cardiomyocyte proliferation compared with supernatant from undisclosed control cells, whereas in primary rat fibroblasts, the Treg-derived supernatant had no effect. In a mouse model of MI, injection of primary mouse Tregs at the infarct site decreased infarct size and increased cardiomyocyte proliferation and cardiac function compared with no treatment. Also in the model, injection at the infarct site of adeno-associated viral serotype 9 (AAV9) vectors encoding RANKL and five other highly expressed Treg factors, or those six factors plus IL-33, IGF-2 and four other highly expressed Treg factors, decreased infarct size and increased cardiomyocyte proliferation and cardiac function compared with empty vectors. Next steps could include identifying the optimal combination of Treg-secreted factors to treat MI...