Letter by Feng and Nie Regarding Article, "Myeloid-Derived Growth Factor Protects Against Pressure Overload-Induced Heart Failure".
Letter by Feng and Nie Regarding Article, "Myeloid-Derived Growth Factor Protects Against Pressure Overload-Induced Heart Failure".
复制标题
DOI：
10.1161/circulationaha.121.057874
复制
发表时间：
2022-03
期刊：
影响因子：
37.8
通讯作者：
Jie Feng;Y. Nie
中科院分区：
文献类型：
--
作者：
Jie Feng;Y. Nie
我们饶有兴趣地阅读了Korf-Klingebiel等人1的文章，该文章阐明了产生MYDGF的单核细胞和巨噬细胞（髓源性生长因子）在压力超负荷心肌中刺激SERCA 2a（肌/内质网钙-ATP酶2a）在心肌细胞中的表达，其增强Ca 2+循环和肌节功能，并在炎性细胞和心肌细胞之间建立基于MYDGF的适应性串扰，并防止压力超负荷引起的心力衰竭。该小组的一项早期研究报告，小鼠和急性心肌梗死患者的血浆MYDGF水平升高，并且MYDGF在心脏修复过程中发挥关键作用（例如，促进心肌梗死后成年小鼠的血管生成和抑制心肌细胞凋亡）。2本研究的发现拓宽了对MYDGF在心脏损伤后修复作用的理解。我们的研究小组还发现，MYDGF通过激活c-Myc（myc原癌基因，BHLH转录因子）/FoxM 1（叉头盒M1）途径促进心肌细胞增殖，改善新生和成年小鼠心脏损伤后的心脏再生。3由于促进内源性心肌细胞增殖可以使心脏再生取得重大进展，4，5我们问：作者是否检测到MYDGF对压力超负荷诱导的心力衰竭中心肌细胞增殖的影响？目前的研究表明，单核细胞，巨噬细胞和中性粒细胞积累在压力超负荷的左心室心肌，与假手术心脏相比，和MYDGF强烈表达的单核细胞和巨噬细胞。因此，可以得出结论，单核细胞和巨噬细胞是主要的Mydgf表达免疫细胞类型。压力超负荷心肌中单核细胞和巨噬细胞表达的MYDGF是否高于假手术心肌。作者应用共聚焦免疫荧光显微镜，
We read with interest the article by Korf-Klingebiel et al1 illustrating that the monocytes and macrophages producing MYDGF (myeloid-derived growth factor) in pressure-overloaded myocardium stimulate SERCA2a (sarco/endoplasmic reticulum calcium-ATPase 2a) expression in cardiomyocytes, which augments Ca2+ cycling and sarcomere function and establishes an MYDGF-based adaptive crosstalk between inflammatory cells and cardiomyocytes, and protects against pressure overload–induced heart failure. An earlier study by this group reported that the plasma level of MYDGF is elevated in mice and patients with acute myocardial infarction and that MYDGF plays a crucial role during cardiac repair (eg, promoting angiogenesis and inhibiting cardiomyocyte apoptosis in adult mice post myocardial infarction). 2 The findings of the current study broaden the understanding of the reparative effects of MYDGF after heart injury. Our group has also revealed that MYDGF promotes cardiomyocyte proliferation by activating the c-Myc (myc proto-oncogene, BHLH transcription factor)/FoxM1 (forkhead box M1) pathway, improving heart regeneration both in neonatal and adult mice after cardiac injury. 3 Because promoting endogenous cardiomyocyte proliferation could enable major advances in cardiac regeneration, 4, 5 we ask: Did the authors detect the effects of MYDGF on cardiomyocyte proliferation in pressure overload–induced heart failure?The current study showed that monocytes, macrophages, and neutrophils accumulated in the pressure-overloaded left ventricle myocardium, compared with sham-operated hearts, and MYDGF was strongly expressed by monocytes and macrophages. Thus, it was concluded that monocytes and macrophages were the main Mydgf-expressing immune cell types. A question proposed whether the MYDGF expressed by monocytes and macrophages in the pressure-overloaded myocardium was more than that in sham-operated hearts. The authors applied confocal immunofluorescence micros-