Dipeptidyl peptidase-4 deficiency prevents chronic stress-induced cardiac remodeling and dysfunction in mice.

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Tác giả: Xian Wu Cheng, Rihua Cui, Zhe Jiang, Xianglan Jin, Weon Kim, Yanglong Li, Ying Wan, Hongxian Wu, Minglong Xin, Shengnan Xu, Xueling Yue, Longguo Zhao

Ngôn ngữ: eng

Ký hiệu phân loại: 518.6 Numerical methods in analysis

Thông tin xuất bản: United States : FASEB journal : official publication of the Federation of American Societies for Experimental Biology , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 215577

Exposure to chronic psychosocial stress is a risk factor for metabolic cardiovascular disorders. Dipeptidyl peptidase-4 (DPP-4) plays essential roles in human pathobiology, and we recently showed that DPP-4 levels are increased by chronic stress in murine models. We here investigated the role of DPP-4 in stress-related cardiac injury and dysfunction in mice, focusing on oxidative stress and cardiac apoptosis. Male mice were randomly assigned to non-stress and two-week immobilized-stress groups for biological and morphological studies. On day 14 post-stress, stress had increased blood pressure, heart weight, cardiac myocyte size, and interstitial fibrosis, impaired cardiac diastolic function, and increased plasma levels of DPP-4 and glucose. The stressed mice also had increased levels of monocyte chemoattractant protein-1, inteleukin-6, gp91
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