KLF4 in smooth muscle cell-derived progenitor cells is essential for angiotensin II-induced cardiac inflammation and fibrosis.

This article discusses the role of a specific protein called KLF4 in the development of cardiac fibrosis, which is characterized by the excessive accumulation of scar tissue in the heart. The study found that a subpopulation of resident vascular stem cells, called AdvSca1-SM cells, originate from mature vascular smooth muscle cells through a process called in situ reprogramming. The researchers used genetic knockout techniques to show that KLF4 is essential for the profibrotic response of AdvSca1-SM cells. These findings suggest that KLF4 could be a potential therapeutic target for treating cardiac fibrosis. However, it is important to note that this study has not yet undergone peer review. [Extracted from the article]