Letter by Feng and Nie Regarding Article, "Myeloid-Derived Growth Factor Protects Against Pressure Overload-Induced Heart Failure".

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HomeCirculationVol. 145, No. 11Letter by Feng and Nie Regarding Article, “Myeloid-Derived Growth Factor Protects Against Pressure Overload-Induced Heart Failure” Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessLetterPDF/EPUBLetter by Feng and Nie Regarding Article, “Myeloid-Derived Growth Factor Protects Against Pressure Overload-Induced Heart Failure” Jie Feng, PhD and Yu Nie, PhD Jie FengJie Feng State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing. Search for more papers by this author and Yu NieYu Nie https://orcid.org/0000-0002-8744-0046 State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing. Search for more papers by this author Originally published14 Mar 2022https://doi.org/10.1161/CIRCULATIONAHA.121.057874Circulation. 2022;145:e768–e769To the Editor: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 microscopy delineating MYDGF-expressing cells in the pressure-overloaded left ventricle and found 57±4% of the MYDGF-expressing cells coexpressed the myeloid cell marker CD11b. The finding suggested there was still a large amount of MYDGF expressed by other cell types, which cannot be ignored.In addition, in their Figure 1E, the authors showed that MYDGF-expressing cells coexpressed with the myeloid cell marker CD11b (cluster of differentiation molecule 11b) and no MYDGF immunofluorescence signal were detected in Mydgf-knockout mice. However, group information was missing in Figure 1E. Are the data at the bottom from Mydgf-knockout heart? If so, it is interesting that Mydgf-knockout seems to result in increased myeloid cells (red marked): Could the authors provide interpretation for it?Article InformationSources of FundingThis study was supported by the National Key Research and Development Project of China (2019YFA0801500) and the National Natural Science Foundation of China (81770308; 81970243).Disclosures None.FootnotesCirculation is available at www.ahajournals.org/journal/circ