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Background Hypertension induces end-organ damage through inflammation, and autophagy plays a crucial role in the regulation of cellular homeostasis, but the role of autophagy in hypertension induced cardiac injury is still unclear.Objective In the present study, we aimed to define the role of autophagy in the development of inflammation and cardiac injury induced by angiotensin Ⅱ (Ang Ⅱ) through autophagy associated gene Atg 5.Methods Autophagy protein 5 (Atg5) haplodeficiency (Atg5(+/-) and age-matched wild-type (WT) C57BL/6J mice were infused with Ang Ⅱ (1500ng/kg/min) or saline for 7 days.Heart sections were stained with hematoxylin and eosin (H&E), Massons trichrome, and immune-histochemical stains.Cytokine and LC3 levels were measured using real-time PCR or western blot analysis.Results After Ang Ⅱinfusion, the WT mice exhibited marked macrophage accumulation, Atg 5 expression in macrophages, and reactive oxygen species (ROS) production compared with saline-infused controls.However, these effects induced by Ang Ⅱ infusion were aggravated in Atg 5 (+/-) mice.These effects were associated with Atg5-mediated impaired autophagy, accompanied by increased production of ROS and activation of nuclear factor-κB (NF-κB) in macrophages.Finally, increased cardiac inflammation in Atg 5 (+/-) mice was associated with increased cardiac fibrosis.Conclusion Atg 5 deficiency-mediated autophagy increases ROS production and NF-κB activity in macrophages, thereby contributing to cardiac inflammation and injury.Thus, improving autophagy may be a novel therapeutic strategy to ameliorate hypertension-induced inflammation and organ damage.