加拿大多伦大学Slava Epelman研究组发现，驻留巨噬细胞来源胰岛素样生长因子1的选择性丧失阻碍心脏对压力的适应性增长。相关论文于2021年8月6日在线发表于国际学术期刊《免疫》。

研究人员发现，在正常血压的动物中，自我更新的心脏常驻巨噬细胞（RM）的单细胞转录组学显示了转录多样化的细胞状态，具有修复性基因程序的核心特征，包括胰岛素样生长因子1（Igf1）的高表达。高血压推动了一些心脏RM状态的选择性原位增殖和转录激活，与心肌细胞的增长直接相关。在高血压期间，RM的诱导性敲除或选择性地删除RM衍生的Igf1阻止了心肌细胞的适应性生长，心脏质量未能增加，从而导致心脏功能紊乱。

单细胞转录组学确定了人类心肌病中保守的表达IGF1的巨噬细胞亚群。因此，研究人员确定了RM产生的IGF-1在心脏适应高血压方面的绝对需求。

据悉，高血压影响了世界三分之一的人口，导致心脏功能障碍，而这种障碍是由驻留和招募的免疫细胞所调节。心肌细胞的生长和心脏质量的增加是承受高血压压力的必要条件；然而，免疫细胞是否参与这种补偿性的心脏保护过程尚不清楚。

附：英文原文

Title: Selective loss of resident macrophage-derived insulin-like growth factor-1 abolishes adaptive cardiac growth to stress

Author: Rysa Zaman, Homaira Hamidzada, Crystal Kantores, Anthony Wong, Sarah A. Dick, Yiming Wang, Abdul Momen, Laura Aronoff, Julia Lin, Babak Razani, Seema Mital, Filio Billia, Kory J. Lavine, Sara Nejat, Slava Epelman

Issue&Volume: 2021-08-06

Abstract: Hypertension affects one-third of the world’s population, leading to cardiac dysfunctionthat is modulated by resident and recruited immune cells. Cardiomyocyte growth andincreased cardiac mass are essential to withstand hypertensive stress; however, whetherimmune cells are involved in this compensatory cardioprotective process is unclear.In normotensive animals, single-cell transcriptomics of fate-mapped self-renewingcardiac resident macrophages (RMs) revealed transcriptionally diverse cell stateswith a core repertoire of reparative gene programs, including high expression of insulin-likegrowth factor-1 (Igf1). Hypertension drove selective in situ proliferation and transcriptional activation of some cardiac RM states, directlycorrelating with increased cardiomyocyte growth. During hypertension, inducible ablationof RMs or selective deletion of RM-derived Igf1 prevented adaptive cardiomyocyte growth, and cardiac mass failed to increase, whichled to cardiac dysfunction. Single-cell transcriptomics identified a conserved IGF1-expressing macrophage subpopulation in human cardiomyopathy. Here we defined theabsolute requirement of RM-produced IGF-1 in cardiac adaptation to hypertension.

DOI: 10.1016/j.immuni.2021.07.006

Source: https://www.cell.com/immunity/fulltext/S1074-7613(21)00292-2