Letter by Wang et al Regarding Article, “Visceral Adipose Tissue Drives Cardiac Aging Through Modulation of Fibroblast Senescence by Osteopontin Production”

HomeCirculationVol. 139, No. 6Letter by Wang et al Regarding Article, "Visceral Adipose Tissue Drives Cardiac Aging Through Modulation of Fibroblast Senescence by Osteopontin Production" Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBLetter by Wang et al Regarding Article, "Visceral Adipose Tissue Drives Cardiac Aging Through Modulation of Fibroblast Senescence by Osteopontin Production" Daxin Wang, MD, Xinquan Yang, MD and Yan Dai, PhD Daxin WangDaxin Wang Clinical Medical College, Yangzhou University, Yangzhou, Jiangsu, China (D.W., X.Y., Y.D.). , Xinquan YangXinquan Yang Clinical Medical College, Yangzhou University, Yangzhou, Jiangsu, China (D.W., X.Y., Y.D.). Department of Cardiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China (X.Y.). and Yan DaiYan Dai Clinical Medical College, Yangzhou University, Yangzhou, Jiangsu, China (D.W., X.Y., Y.D.). Originally published4 Feb 2019https://doi.org/10.1161/CIRCULATIONAHA.118.035262Circulation. 2019;139:843–844To the Editor:We carefully read with interest the recent article by Sawaki and colleagues,1 in which they suggested visceral adipose tissue (VAT) as the main source of osteopontin and that VAT could alter the structure and function of the heart via modulation of fibroblast senescence during aging. Their results established and clarified the important role of VAT in age-related cardiac remodeling, which may be beneficial in discovering a novel therapy for patients with heart failure with preserved ejection fraction (HFpEF). As the authors discussed, there was a remarkable increase in the secretion of profibrotic factors in VAT. What are the effects and mechanism of physiological aging on such a phenomenon in VAT? According to the results presented by Dr Sawaki and team, there was no significant change in systemic insulin resistance between the sham and epididymal fat resection mice groups. Moreover, a negligible increase was observed with respect to the expression of the usual inflammatory markers in VAT. Obesity is currently considered to be the most frequent comorbidity in patients with HFpEF, and systemic inflammation has been proposed as a fundamental mechanism that leads to deterioration of HFpEF.2 Nevertheless, interruption of the inflammatory signals in VAT could potentially reduce systemic inflammation and insulin resistance and ameliorate cardiac function in the setting of chronic heart failure.3 In addition, immunometabolic anomalies were suggested to play a crucial role in VAT inflammation and insulin resistance under the condition of obesity through osteopontin production.4 Therefore, we would like to know whether the reduction or even inhibition of osteopontin generation in VAT could exert protective effects on antiremodeling in a heart failure model or a heart failure combined with obesity model. More important, a previous study has demonstrated that abdominal obesity in patients with HFpEF was significantly associated with higher risks of all-cause mortality.5 Hence, it is of profound importance to find an effective strategy to reduce the mortality risk of patients with HFpEF. A deeper understanding of the relationship between inflammation and the production of osteopontin in VAT could shed some light on and clarify the effects of osteopontin in the complicated heart failure background and bring it closer to clinical application.DisclosuresNone.Footnoteshttps://www.ahajournals.org/journal/circReferences1. Sawaki D, Czibik G, Pini M, Ternacle J, Suffee N, Mercedes R, Marcelin G, Surenaud M, Marcos E, Gual P, Clément K, Hue S, Adnot S, Hatem SN, Tsuchimochi I, Yoshimitsu T, Hénégar C, Derumeaux G. Visceral adipose tissue drives cardiac aging through modulation of fibroblast senescence by osteopontin production.Circulation. 2018; 138:809–822. doi: 10.1161/CIRCULATIONAHA.117.031358LinkGoogle Scholar2. Redfield MM. Heart failure with preserved ejection fraction.N Engl J Med. 2016; 375:1868–1877. doi: 10.1056/NEJMcp1511175CrossrefMedlineGoogle Scholar3. Shimizu I, Yoshida Y, Katsuno T, Tateno K, Okada S, Moriya J, Yokoyama M, Nojima A, Ito T, Zechner R, Komuro I, Kobayashi Y, Minamino T. p53-Induced adipose tissue inflammation is critically involved in the development of insulin resistance in heart failure.Cell Metab. 2012; 15:51–64. doi: 10.1016/j.cmet.2011.12.006CrossrefMedlineGoogle Scholar4. Shirakawa K, Yan X, Shinmura K, Endo J, Kataoka M, Katsumata Y, Yamamoto T, Anzai A, Isobe S, Yoshida N, Itoh H, Manabe I, Sekai M, Hamazaki Y, Fukuda K, Minato N, Sano M. Obesity accelerates T cell senescence in murine visceral adipose tissue.J Clin Invest. 2016; 126:4626–4639. doi: 10.1172/JCI88606CrossrefMedlineGoogle Scholar5. Tsujimoto T, Kajio H. Abdominal obesity is associated with an increased risk of all-cause mortality in patients with HFpEF.J Am Coll Cardiol. 2017; 70:2739–2749. doi: 10.1016/j.jacc.2017.09.1111CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails February 5, 2019Vol 139, Issue 6 Advertisement Article InformationMetrics © 2019 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.118.035262PMID: 30715948 Originally publishedFebruary 4, 2019 PDF download Advertisement SubjectsBasic Science ResearchHeart FailureMetabolismObesityRemodeling