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• W4382810618 abstract "Abstract Diabetic cardiomyopathy (DCM) is one of the main complications in type I diabetic patients. Activated macrophage is critical for directing the process of inflammation during the development of DCM. The present study focused on the roles of CD226 on macrophage function during the DCM progression. It has been found that the number of cardiac macrophages in the hearts of streptozocin (STZ)‐induced diabetes mice was significantly increased compared with that in non‐diabetes mice, and the expression level of CD226 on cardiac macrophages in STZ‐induced diabetes mice was higher than that in non‐diabetes mice. CD226 deficiency attenuated the diabetes‐induced cardiac dysfunction and decreased the proportion of CD86 + F4/80 + macrophages in the diabetic hearts. Notably, adoptive transfer of Cd226 −/− ‐ bone marrow derived macrophages (BMDMs) alleviated diabetes‐induced cardiac dysfunction, which may be due to the attenuated migration capacity of Cd226 −/− ‐BMDM under high glucose stimulation. Furthermore, CD226 deficiency decreased the macrophage glycolysis accompanying by the downregulated hexokinase 2 (HK2) and lactate dehydrogenase A (LDH‐A) expression. Taken together, these findings revealed the pathogenic roles of CD226 played in the process of DCM and provided a basis for the treatment of DCM." @default.
• W4382810618 created "2023-07-02" @default.
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• W4382810618 date "2023-07-01" @default.
• W4382810618 modified "2023-10-17" @default.
• W4382810618 title "CD226 deficiency attenuates cardiac early pathological remodeling and dysfunction via decreasing inflammatory macrophage proportion and macrophage glycolysis in <scp>STZ</scp>‐induced diabetic mice" @default.
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• W4382810618 doi "https://doi.org/10.1096/fj.202300424rr" @default.
• W4382810618 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37392373" @default.
• W4382810618 hasPublicationYear "2023" @default.
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