脂肪组织
腹主动脉瘤
炎症
医学
主动脉瘤
肥胖
内科学
心脏病学
病理
动脉瘤
放射科
作者
Qing Zhu,Da Luo,Yining Li,Liyang Yu,Zixuan Zhang,Feng Ouyang,Liangkui Li,Manxi Lu,Changyong Hu,Yinuo Dong,Chengxin Ma,Yan Liang,Tong‐Jin Zhao,Feng‐Jung Chen,Peng Li,Tianshu Yang
标识
DOI:10.1093/lifemeta/loae035
摘要
Abstract Abdominal aortic aneurysm (AAA) is strongly correlated with obesity, partially due to the abnormal expansion of abdominal perivascular adipose tissue (PVAT). Cell death-inducing DNA fragmentation factor-like effector C (CIDEC), also known as fat-specific protein 27 (FSP27) in rodents, is specifically expressed in adipose tissue where it mediates lipid droplet fusion and adipose tissue expansion. Whether and how CIDEC/FSP27 plays a role in AAA pathology remains elusive. Here, we show that FSP27 exacerbates obesity and angiotensin II (Ang II)-induced AAA progression. FSP27 deficiency in mice inhibited high-fat diet (HFD)-induced PVAT expansion and inflammation. Both global and adipose tissue-specific FSP27 ablation significantly decreased obesity-related AAA incidence. Deficiency of FSP27 in adipocytes abrogated matrix metalloproteinase-12 (MMP12) expression in aortic tissues. Infiltrated macrophages, which partially colocalize with MMP12, were significantly decreased in the FSP27-deficient aorta. Mechanistically, knockdown of Fsp27 in 3T3-L1 adipocytes inhibited C-C motif chemokine ligand 2 (CCL2) expression and secretion through a c-Jun N-terminal kinase (JNK)-dependent pathway, thereby leading to reduced induction of macrophage migration, while Cidec overexpression rescued this effect. Overall, our study demonstrates that CIDEC/FSP27 in adipose tissue contributes to obesity-related AAA formation, at least in part, by enhancing PVAT inflammation and macrophage infiltration, thus shedding light on its significance as a key regulator in the context of obesity-related AAA.
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