Endo, Jin

写真a

Affiliation

School of Medicine, Department of Internal Medicine (Cardiology) (Shinanomachi)

Position

Assistant Professor/Senior Assistant Professor
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Papers 【 Display / hide 】

  • Biventricular takotsubo cardiomyopathy with asymmetrical wall motion abnormality between left and right ventricle: a report of new case and literature review

    Tsugu T., Nagatomo Y., Nakajima Y., Kageyama T., Endo J., Itabashi Y., Kawakami T.

    Journal of Echocardiography (Journal of Echocardiography)  17 ( 3 ) 123 - 128 2019.09

    ISSN  13490222

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    © 2019, Japanese Society of Echocardiography. Takotsubo cardiomyopathy (TC) is characterized by transient wall motion abnormalities most commonly involving the left ventricle (LV). Although biventricular TC had been considered uncommon condition, recently biventricular TC has been reported as a new variant observed in 19–42% of all TC presentations. Since biventricular TC has a poor prognosis as compared with isolated TC, it is important to distinguish between isolated LV TC and biventricular TC. We present a case of 70-year-old female with dyspnea persisting for 2 days. Electrocardiogram showed symmetrical T-wave inversion in leads V2–V4. Transthoracic echocardiography (TTE) revealed diffuse hypo-kinesis except for the apical inferior LV and LV ejection fraction of 32%. Hyper-kinesis of the right ventricular (RV) basal segment and dys-kinesis of the RV apical segment. 2 weeks after admission, coronary angiography showed no evidence of significant stenosis. LV ejection fraction improved to 51% and wall motion abnormalities of the RV basal and apical segments were ameliorated to normo-kinesis. Electrocardiogram revealed symmetrical and deepened T-wave inversion in leads V2–V3. The presence of a transient abnormality in biventricular wall motion beyond a single coronary artery perfusion territory with new electrocardiographic change met the diagnostic criteria of definite TC defined by Mayo Clinic criteria. 4 weeks after admission, no recurrence of wall motion abnormalities in both ventricles were found and T-wave inversion ameliorated. To our knowledge, this is the first report of biventricular TC with asymmetrical abnormities of wall motion between LV and RV.

  • Sirt1 counteracts decrease in membrane phospholipid unsaturation and diastolic dysfunction during saturated fatty acid overload

    Yamamoto T., Endo J., Kataoka M., Matsuhashi T., Katsumata Y., Shirakawa K., Yoshida N., Isobe S., Moriyama H., Goto S., Yamashita K., Ohto-Nakanishi T., Nakanishi H., Shimanaka Y., Kono N., Shinmura K., Arai H., Fukuda K., Sano M.

    Journal of Molecular and Cellular Cardiology (Journal of Molecular and Cellular Cardiology)  133   1 - 11 2019.08

    ISSN  00222828

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    © 2019 Elsevier Ltd Background: The fatty acid (FA)composition of membrane phospholipid reflects at least in part dietary fat composition. Saturated FA (SFA)suppress Sirt1 activity, while monounsaturated FA (MUFA)counteract this effect. Objective: We explored a role of Sirt1 in homeostatic control of the fatty acid composition of membrane phospholipid in the presence of SFA overload. Methods and results: Sirt1 deficiency in cardiomyocytes decreased the expression levels of liver X receptor (LXR)-target genes, particularly stearoyl-CoA desaturase-1 (Scd1), a rate-limiting enzyme in the cellular synthesis of MUFA from SFA, increased membrane SFA/MUFA ratio, and worsened left ventricular (LV)diastolic function in mice fed an SFA-rich high fat diet. In cultured cardiomyocytes, Sirt1 knockdown (KD)exacerbated the palmitate overload-induced increase in membrane SFA/MUFA ratio, which was associated with decrease in the expression of LXR-target genes, including Scd1. Forced overexpression of Scd1 in palmitate-overloaded Sirt1KD cardiomyocytes lowered the SFA/MUFA ratio. Nicotinamide mononucleotide (NMN)increased Sirt1 activity and Scd1 expression, thereby lowering membrane SFA/MUFA ratio in palmitate-overloaded cardiomyocytes. These effects of NMN were not observed for Scd1KD cardiomyocytes. LXRα/βKD exacerbated palmitate overload-induced increase in membrane SFA/MUFA ratio, while LXR agonist T0901317 alleviated it. NMN failed to rescue Scd1 protein expression and membrane SFA/MUFA ratio in palmitate-overloaded LXRα/βKD cardiomyocytes. The administration of NMN or T0901317 showed a dramatic reversal in membrane SFA/MUFA ratio and LV diastolic function in SFA-rich HFD-fed mice. Conclusion: Cardiac Sirt1 counteracted SFA overload-induced decrease in membrane phospholipid unsaturation and diastolic dysfunction via regulating LXR-mediated transcription of the Scd1 gene.

  • Multiple papillary fibroelastomas attached to left ventricular side and aortic side of the aortic valve: A report of new case and literature review

    Tsugu T., Nagatomo Y., Endo J., Kawakami T., Murata M., Yamazaki M., Shimizu H., Fukuda K., Mitamura H., Lancellotti P.

    Echocardiography (Echocardiography)  36 ( 6 ) 1194 - 1199 2019.06

    ISSN  07422822

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    © 2019 Wiley Periodicals, Inc. The aortic valve (AV) is the most commonly affected site in multiple papillary fibroelastomas, but the frequency of embolism caused by the attachment side of the AV has not been elucidated. According to the review of the previous literature, 16 cases have been found attached to the AV. Of these, 6 of these have been found to be attached on the aortic side and 4 on the left ventricular side, 1 was bilateral, and 5 cases were unknown. Of the cases found on the aortic side, embolism occurred in 3 of them, and of the left ventricular side cases, embolism occurred in 2 of them. The frequency of embolism is equivalent even if papillary fibroelastoma attached to either side of the AV.

  • Pressure overload inhibits glucocorticoid receptor transcriptional activity in cardiomyocytes and promotes pathological cardiac hypertrophy

    Matsuhashi T., Endo J., Katsumata Y., Yamamoto T., Shimizu N., Yoshikawa N., Kataoka M., Isobe S., Moriyama H., Goto S., Fukuda K., Tanaka H., Sano M.

    Journal of Molecular and Cellular Cardiology (Journal of Molecular and Cellular Cardiology)  130   122 - 130 2019.05

    ISSN  00222828

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    © 2019 Glucocorticoid receptor (GR) is abundantly expressed in cardiomyocytes. However, the role of GR in regulating cardiac hypertrophy and heart failure in response to pressure overload remains unclear. Cardiomyocyte-specific GR knockout (GRcKO) mice, mineralocorticoid receptor (MR) knockout (MRcKO), and GR and MR double KO (GRMRdcKO) mice were generated using the Cre-lox system. In response to pressure overload, GRcKO mice displayed worse cardiac remodeling compared to control (GR f/f ) mice, including a greater increase in heart weight to body weight ratio with a greater increase in cardiomyocytes size, a greater decline in left ventricular contractility, and higher reactivation of fetal genes. MRcKO mice showed a comparable degree of cardiac remodeling compared to control (MR f/f ) mice. The worse cardiac remodeling in pressure overloaded GRcKO mice is not due to compensatory activation of cardiomyocyte MR, since pressure overloaded GRMRdcKO mice displayed cardiac remodeling to the same extent as GRcKO mice. Pressure overload suppressed GR-target gene expression in the heart. Although plasma corticosterone levels and subcellular localization of GR (nuclear/cytoplasmic GR) were not changed, a chromatin immunoprecipitation assay revealed that GR recruitment onto the promoter of GR-target genes was significantly suppressed in response to pressure overload. Rescue of the expression of GR-target genes to the same extent as sham-operated hearts attenuated adverse cardiac remodeling in pressure-overloaded hearts. Thus, GR works as a repressor of adverse cardiac remodeling in response to pressure overload, but GR-mediated transcription is suppressed under pressure overload. Therapies that maintain GR-mediated transcription in cardiomyocytes under pressure overload can be a promising therapeutic strategy for heart failure.

  • Cancer therapeutics-related cardiac dysfunction in a patient treated with abiraterone for castration-resistant prostate cancer

    Tsugu T., Nagatomo Y., Nakajima Y., Kageyama T., Akise Y., Endo J., Itabashi Y., Murata M., Mitamura H.

    Journal of Medical Ultrasonics (Journal of Medical Ultrasonics)  46 ( 2 ) 239 - 243 2019.04

    ISSN  13464523

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    © 2018, The Japan Society of Ultrasonics in Medicine. Abiraterone is an agent effective for castration-resistant prostate cancer, but there have been no reports of cardiotoxic effects inducing cardiomyopathy, to our knowledge. We present a case of an 86-year-old man with castration-resistant prostate cancer treated with abiraterone. He had received an androgen receptor antagonist (bicalutamide) and a gonadotropin-releasing hormone antagonist (degarelix) for 3 years. These agents were changed to enzalutamide due to elevation of plasma prostate-specific antigen level of 129 ng/mL. One year later, the oral androgen receptor inhibitor (enzalutamide) caused drug-induced lung injury and was changed to abiraterone. Transthoracic echocardiography (TTE) revealed normal left ventricular systolic function, and left ventricular ejection fraction (LVEF) was 67%. Four weeks after administration of abiraterone, he complained of dyspnea on effort and bilateral leg edema, and he was diagnosed with heart failure. TTE showed hypokinesis of the diffuse LV, and LVEF decreased to 45%. The various causes of heart failure were excluded. Since a cardiotoxic effect of abiraterone was suspected, administration of abiraterone was discontinued. Two weeks after cessation of abiraterone, LVEF ameliorated to 57%, and then 5 months after cessation of abiraterone, LVEF further improved to 65%. To our knowledge, this is the first report of definite cancer therapeutics-related cardiac dysfunction due to a hormonal agent such as abiraterone diagnosed according to the American Society of Echocardiography and European Association of Cardiovascular Imaging criteria.

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Papers, etc., Registered in KOARA 【 Display / hide 】

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Reviews, Commentaries, etc. 【 Display / hide 】

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Research Projects of Competitive Funds, etc. 【 Display / hide 】

  • Elucidation of the pathogenic mechanism of ATTRwt amyloidosis

    2024.04
    -
    2027.03

    基盤研究(B), Principal investigator

  • ミトコンドリア制御蛋白を介した心筋保護機構の解明および新規治療法の開発

    2021.04
    -
    2024.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), Principal investigator

  • サルコペニアの新規分子機構の解明と治療戦略の創出

    2018.04
    -
    2021.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), Principal investigator

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Courses Taught 【 Display / hide 】

  • LECTURE SERIES, INTERNAL MEDICINE (CARDIOLOGY)

    2024

  • LECTURE SERIES, INTERNAL MEDICINE (CARDIOLOGY)

    2023

  • INTRODUCTION TO CLINICAL CLERKSHIPS

    2023

  • LECTURE SERIES, INTERNAL MEDICINE (CARDIOLOGY)

    2022

  • INTRODUCTION TO CLINICAL CLERKSHIPS

    2022

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