Atherosclerosis, a chronic inflammatory condition primarily affecting large and medium arteries, is the main cause of cardiovascular diseases. Macrophages are key mediators of inflammatory responses. They are involved in all stages of atherosclerosis development and progression, from plaque formation to transition into vulnerable plaques, and are considered important therapeutic targets. Increasing evidence suggests that the modulation of macrophage polarization can effectively control the progression of atherosclerosis. Herein, we explore the role of macrophage polarization in the progression of atherosclerosis and summarize emerging therapies for the regulation of macrophage polarization. Thus, the aim is to inspire new avenues of research in disease mechanisms and clinical prevention and treatment of atherosclerosis.

Background Extracellular vesicles (EVs) are a popular treatment candidate for myocardial injury. This work investigated the effects of mesenchymal stem cells (MSCs)–secreted EVs–derived miR‐200b‐3p on cardiomyocyte apoptosis and inflammatory response after myocardial infarction (MI) through targeting BCL2L11 (Bcl‐2–like protein 11) . Methods and Results EVs from MSCs were isolated and identified. EVs from MSCs with transfection of miR‐200b‐3p for overexpression were injected into MI mice. The effect of miR‐200b‐3p on cardiac function, infarction area, myocardial fibrosis, cardiomyocyte apoptosis, and inflammatory response was determined in MI mice. The targeting relationship between miR‐200b‐3p and BCL2L11 was verified, and the interaction between BCL2L11 and NLR family pyrin domain containing 1 (NLRP1) was also verified. MI mice were injected with an overexpressing BCL2L11 lentiviral vector to clarify whether BCL2L11 can regulate the effect of miR‐200b‐3p on MI mice. EVs from MSCs were successfully extracted. MSCs‐EVs improved cardiac function and reduced infarction area, apoptosis of cardiomyocytes, myocardial fibrosis, and inflammation in MI mice. Upregulation of miR‐200b‐3p further enhanced the effects of MSCs‐EVs on the myocardial injury of MI mice. BCL2L11 was targeted by miR‐200b‐3p and bound to NLRP1. Upregulation of BCL2L11 negated the role of miR‐200b‐3p–modified MSCs‐EVs in MI mice. Conclusions A summary was obtained that miR‐200b‐3p–encapsulated MSCs‐EVs protect against MI‐induced apoptosis of cardiomyocytes and inflammation via suppressing BCL2L11.

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