在这项工作中，研究团队研究了小鼠米色脂肪，作为人类诱导棕色脂肪的模型，在脂肪细胞-血管串扰中的作用。使用脂肪细胞特异性Prdm16敲除小鼠，失去米色脂肪细胞的特性，该研究组发现血管周围脂肪组织的显著重塑，血管反应性增加，血压升高。该团队发现循环酶QSOX1在缺乏Prdm16的脂肪细胞中被抑制，并且在Prdm16条件敲除小鼠中QSOX1的缺失阻止了血管纤维化和血管反应性的正常化。这些结果证明了米色脂肪细胞在血压调节中的关键作用，并确定了QSOX1是脂肪细胞-血管串扰的重要介质。
据悉，过度肥胖是高血压和心脏病的主要危险因素。棕色脂肪与预防心血管疾病有关，但这种关系是否为因果关系尚不清楚。
附：英文原文
Title: Ablation of Prdm16 and beige fat identity causes vascular remodeling and elevated blood pressure
Author: Mascha Koenen, Tobias Becher, Giulia Pagano, Ilaria Del Gaudio, Jorge A. Barrero, Augusto C. Montezano, Jenelys Ruiz Ortiz, Zeran Lin, Nicolás Gómez-Banoy, Rose Amblard, Daniel Schriever, Meltem E. Kars, Luisa Rubinelli, Sarah J. Halix, Zhen Fang Huang Cao, Xing Zeng, Scott D. Butler, Yuval Itan, Rhian M. Touyz, Annarita Di Lorenzo, Paul Cohen
Issue&Volume: 2026-01-15
Abstract: Excess adiposity is a major risk factor for hypertension and heart disease. Brown fat is associated with protection from cardiovascular pathology, but whether this relationship is causal remains unknown. In this work, we investigate the role of mouse beige fat, as a model of human inducible brown fat, in adipocyte-vascular cross-talk. Using adipocyte-specific Prdm16 knockout mice with a loss of beige adipocyte identity, we discovered marked remodeling of perivascular adipose tissue, increased vascular reactivity, and elevated blood pressure. We show that the circulating enzyme QSOX1 is derepressed in Prdm16-deficient adipocytes, and deletion of Qsox1 in Prdm16 conditional knockout mice prevented vascular fibrosis and normalized vascular reactivity. These results demonstrate a key role for beige adipocytes in blood pressure regulation and identify QSOX1 as an important mediator of adipocyte-vascular cross-talk.
DOI: ady8644
Source: https://www.science.org/doi/10.1126/science.ady8644