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血管生成脂肪因子 C1q-TNF 相关蛋白 9 通过组蛋白去乙酰化酶 7 介导的 MEF2 激活改善心肌梗死。

Angiogenic adipokine C1q-TNF-related protein 9 ameliorates myocardial infarction via histone deacetylase 7-mediated MEF2 activation.

机构信息

Department of Convergence Medicine and Asan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.

Convergence Medicine Research Center (CREDIT), Asan Institute for Life Sciences, Asan Medical Center, Seoul, Republic of Korea.

出版信息

Sci Adv. 2022 Dec 2;8(48):eabq0898. doi: 10.1126/sciadv.abq0898.

DOI:10.1126/sciadv.abq0898
PMID:36459558
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10936044/
Abstract

C1q/tumor necrosis factor-related protein 9 (CTRP9) is an adipokine and has high potential as a therapeutic target. However, the role of CTRP9 in cardiovascular disease pathogenesis remains unclear. We found CTRP9 to induce HDAC7 and p38 MAPK phosphorylation via tight regulation of AMPK in vascular endothelial cells, leading to angiogenesis through increased activity. The expression of and atheroprotective was decreased in plaque tissue of atherosclerotic patients and the ventricle of post-infarction mice. CTRP9 treatment inhibited the formation of atherosclerotic plaques in ApoE KO and CTRP9 KO mice. In addition, CTRP9 induced significant ischemic injury prevention in the post-MI mice. Clinically, serum CTRP9 levels were reduced in patients with MI compared with healthy controls. In summary, CTRP9 induces a vasoprotective response via the AMPK/HDAC7/p38 MAPK pathway in vascular endothelial cells, whereas its absence can contribute to atherosclerosis and MI. Hence, CTRP9 may represent a valuable therapeutic target and biomarker in cardiovascular diseases.

摘要

C1q/肿瘤坏死因子相关蛋白 9（CTRP9）是一种脂肪因子，具有作为治疗靶点的巨大潜力。然而，CTRP9 在心血管疾病发病机制中的作用尚不清楚。我们发现 CTRP9 通过在血管内皮细胞中对 AMPK 的紧密调节诱导 HDAC7 和 p38 MAPK 磷酸化，从而通过增加 活性促进血管生成。在动脉粥样硬化患者的斑块组织和梗死后小鼠的心室中， 和动脉保护 的表达减少。CTRP9 治疗可抑制 ApoE KO 和 CTRP9 KO 小鼠动脉粥样硬化斑块的形成。此外，CTRP9 可显著预防梗死后小鼠的缺血性损伤。临床上，与健康对照组相比，MI 患者的血清 CTRP9 水平降低。总之，CTRP9 通过血管内皮细胞中的 AMPK/HDAC7/p38 MAPK 通路诱导血管保护性反应，而其缺失可能导致动脉粥样硬化和 MI。因此，CTRP9 可能是心血管疾病有价值的治疗靶点和生物标志物。

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