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Efferocytosis is defined as the clearance of apoptotic cells (ACs) in physiological and pathological states and is performed by efferocytes, such as macrophages. Efferocytosis can lead to the resolution of inflammation and restore tissue homoeostasis; however, the mechanisms of efferocytosis in determining inflammation resolution are still not completely understood, and the effects of efferocytosis on other proresolving properties need to be explored and explained. In this review, the process of efferocytosis will be summarized briefly, and then these mechanisms and effects will be thoroughly discussed. In addition, the association between mechanisms of efferocytosis in determining resolution of inflammation and cardiovascular diseases will also be reviewed, as an understanding of this association may provide information on novel treatment targets. [ABSTRACT FROM AUTHOR]

Increased inflammation is the key mechanism that mediates sepsis induced cardiac injury. Resolvin D1 (RvD1), a bioactive lipid mediator synthesized from docosahexaenoic acid, can attenuate the severity of many inflammation‐related diseases through anti‐inflammatory and pro‐resolving properties. However, the protective role of RvD1 in sepsis induced cardiac injury remains unclear. Mice were randomly divided into three groups: the control group, LPS group and RvD1 + LPS group. LPS (10 mg/kg, i.p.) was used to establish a sepsis‐induced cardiac injury model. RvD1 (5 ug/kg, i.p.) was injected 30 min before LPS injection. RvD1 treatment significantly attenuated the deteriorated cardiac function and cardiac injury induced by LPS, as evidenced by the improved left ventricular ejection fraction, serum levels of cardiac injury markers and severity of cardiomyocyte apoptosis. In addition, RvD1 treatment significantly attenuated the infiltration of pro‐inflammatory M1 macrophages and expression of inflammatory cytokines in the heart. Mechanistically, the attenuated activation of NK‐κB and MAPK signaling mediated the anti‐inflammatory and antiapoptotic effects of RvD1. In addition, LPS‐induced infiltration of neutrophils and M1 macrophages in the spleen was significantly attenuated by the RvD1 treatment. Results of the present study suggest that RvD1 protects the heart against LPS‐induced injuries by attenuating the local and systemic inflammatory response, highlighting the therapeutic effects of RvD1 in sepsis‐induced cardiac injury. [ABSTRACT FROM AUTHOR]