Key result
HMGB1 administration in a mouse model of myocardial infarction activates cardiac stem cells, promotes their differentiation into cardiomyocytes, and improves cardiac function.
Why the study?
Does HMGB1 administration promote cardiac repair and improve cardiac function after myocardial infarction?
Does HMGB1 administration promote cardiac repair and improve cardiac function after myocardial infarction?
This review highlights the potential of HMGB1 as a growth factor-based therapy for cardiac regeneration and repair following myocardial infarction.
Should not yet alter post-MI care; leaves open HMGB1 translation to human cardiac regeneration.
The nuclear protein high-mobility group box 1 (HMGB1) has been largely characterized for its role in inflammation. However, HMGB1 released by inflammatory cells, as well as by necrotic cells, may also act as a signal of tissue damage and participate in tissue repair by recruiting stem cells to the injury site. The emergence of this function has focused the interest on HMGB1 as a molecule with an active role in tissue regeneration. We recently demonstrated that HMGB1 administration in a mouse model of myocardial infarction activates cardiac stem cells and promotes their differentiation into cardiomyocytes. The regenerative effect results in the improvement of cardiac function. In this review, we highlight the beneficial role of HMGB1 and discuss growth factor-based therapeutic approaches for the treatment of myocardial infarction.
No takes yet. Share an insight, caveat, or question.
Germani et al. (2006) conducted a review in Myocardial infarction. High-mobility group box 1 protein (HMGB1) was evaluated. HMGB1 administration in a mouse model of myocardial infarction activates cardiac stem cells, promotes their differentiation into cardiomyocytes, and improves cardiac function.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: