Tranilast for advanced heart failure in patients with muscular dystrophy: a single-arm, open-label, multicenter study

被引：0

作者：

Tsuyoshi Matsumura

Hiroya Hashimoto

Masahiro Sekimizu

Akiko M. Saito

Yasufumi Motoyoshi

Akinori Nakamura

Satoshi Kuru

Takayasu Fukudome

Kazuhiko Segawa

Toshiaki Takahashi

Takuhisa Tamura

Tetsuo Komori

Chigusa Watanabe

Masanori Asakura

Koichi Kimura

Yuko Iwata

机构：

[1] National Hospital Organization Osaka Toneyama Medical Center,Department of Neurology

[2] Nagoya City University Hospital,Clinical Research Management Center

[3] National Hospital Organization Nagoya Medical Center,Clinical Research Center

[4] National Hospital Organization Shimoshizu National Hospital,Department of Neurology

[5] National Hospital Organization Matsumoto Medical Center,Department of Clinical Research

[6] National Hospital Organization Suzuka Hospital,Department of Neurology

[7] National Hospital Organization Nagasaki Kawatana Medical Center,Department of Neurology

[8] National Center of Neurology and Psychiatry,Department of Cardiology

[9] National Hospital Organization Sendai-Nishitaga Hospital,Department of Neurology

[10] National Hospital Organization Higashisaitama National Hospital,Department of Intractable Diseases

[11] National Hospital Organization Hakone Hospital,Department of Neurology

[12] National Hospital Organization Hiroshima-Nishi Medical Center,Department of Neurology

[13] Hyogo College of Medicine,Department of Cardiovascular and Renal Medicine

[14] The University of Tokyo,Department of Laboratory Medicine/Cardiology, The Institute of Medical Science

[15] National Cerebral and Cardiovascular Center Research Institute,Department of Cardiac Physiology

来源：

Orphanet Journal of Rare Diseases | / 17卷

关键词：

Transient receptor potential cation channel subfamily V member 2; Muscular dystrophy; Heart failure; Brain natriuretic peptide; Tranilast;

D O I：

暂无

中图分类号：

学科分类号：

摘要：

引用

共 97 条

[1]

Matsumura T(2011)A longitudinal cause-of-death analysis of patients with Duchenne muscular dystrophy Rinsho Shinkeigaku 51 743-750

[2]

Saito T(2003)TRPV2 is a component of osmotically sensitive cation channels in murine aortic myocytes Circ Res 93 829-838

[3]

Fujimura H(2003)A novel mechanism of myocyte degeneration involving the Ca2+-permeable growth factor—regulated channel J Cell Biol 161 957-967

[4]

Shinno S(2013)Blockade of sarcolemmal TRPV2 accumulation inhibits progression of dilated cardiomyopathy Cardiovasc Res 99 760-768

[5]

Sakoda S(2005)Protective effects of Ca2+ handling drugs against abnormal Ca2+ homeostasis and cell damage in myopathic skeletal muscle cells Biochem Pharmacol 70 740-751

[6]

Muraki K(2009)Dominant-negative inhibition of Ca2+ influx via TRPV2 ameliorates muscular dystrophy in animal models Hum Mol Genet 18 824-834

[7]

Iwata Y(2009)Essential role of TRPV2 ion channel in the sensitivity of dystrophic muscle to eccentric contractions FEBS Lett 583 3600-3604

[8]

Katanosaka Y(2018)Novel inhibitor candidates of TRPV2 prevent damage of dystrophic myocytes and ameliorate against dilated cardiomyopathy in a hamster model Oncotarget 9 14042-14057

[9]

Ito T(2020)Production of TRPV2-targeting functional antibody ameliorating dilated cardiomyopathy and muscular dystrophy in animal models Lab Investig 100 324-337

[10]

Ohya S(2018)A pilot study of tranilast for cardiomyopathy of muscular dystrophy Intern Med 57 311-318

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