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神经调节蛋白-1β改善大鼠尿毒症性心肌病和肾功能障碍。

Neuregulin-1β Improves Uremic Cardiomyopathy and Renal Dysfunction in Rats.

作者信息

Sárközy Márta, Watzinger Simon, Kovács Zsuzsanna Z A, Acar Eylem, Márványkövi Fanni, Szűcs Gergő, Lauber Gülsüm Yilmaz, Galla Zsolt, Siska Andrea, Földesi Imre, Fintha Attila, Kriston András, Kovács Ferenc, Horváth Péter, Kővári Bence, Cserni Gábor, Krenács Tibor, Szabó Petra Lujza, Szabó Gábor Tamás, Monostori Péter, Zins Karin, Abraham Dietmar, Csont Tamás, Pokreisz Peter, Podesser Bruno K, Kiss Attila

机构信息

MEDICS Research Group, Department of Biochemistry, Albert Szent-Györgyi Medical School, University of Szeged, Szeged, Hungary.

Interdisciplinary Center of Excellence, University of Szeged, Szeged, Hungary.

出版信息

JACC Basic Transl Sci. 2023 May 31;8(9):1160-1176. doi: 10.1016/j.jacbts.2023.03.003. eCollection 2023 Sep.

DOI:10.1016/j.jacbts.2023.03.003
PMID:37791301
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10543921/
Abstract

Chronic kidney disease is a global health problem affecting 10% to 12% of the population. Uremic cardiomyopathy is often characterized by left ventricular hypertrophy, fibrosis, and diastolic dysfunction. Dysregulation of neuregulin-1β signaling in the heart is a known contributor to heart failure. The systemically administered recombinant human neuregulin-1β for 10 days in our 5/6 nephrectomy-induced model of chronic kidney disease alleviated the progression of uremic cardiomyopathy and kidney dysfunction in type 4 cardiorenal syndrome. The currently presented positive preclinical data warrant clinical studies to confirm the beneficial effects of recombinant human neuregulin-1β in patients with chronic kidney disease.

摘要

慢性肾脏病是一个全球性的健康问题,影响着10%至12%的人口。尿毒症性心肌病通常表现为左心室肥厚、纤维化和舒张功能障碍。心脏中神经调节蛋白-1β信号失调是导致心力衰竭的一个已知因素。在我们通过5/6肾切除诱导的慢性肾脏病模型中,全身给予重组人神经调节蛋白-1β 10天,可缓解4型心肾综合征中尿毒症性心肌病和肾功能障碍的进展。目前呈现的阳性临床前数据值得进行临床研究,以证实重组人神经调节蛋白-1β对慢性肾脏病患者的有益作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd37/10543921/d81a86d682d6/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd37/10543921/ac81ddf86618/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd37/10543921/ba9a052138ca/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd37/10543921/e009324799ee/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd37/10543921/7c16e30cb815/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd37/10543921/0a3e74bc5959/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd37/10543921/f4d689cc4116/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd37/10543921/d81a86d682d6/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd37/10543921/ac81ddf86618/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd37/10543921/ba9a052138ca/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd37/10543921/e009324799ee/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd37/10543921/7c16e30cb815/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd37/10543921/0a3e74bc5959/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd37/10543921/f4d689cc4116/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd37/10543921/d81a86d682d6/gr6.jpg

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