Research Advances in the Mechanisms of Hyperuricemia-Induced Renal Injury

المؤلفون المشاركون

Liu, Hua-feng
Su, Hong-yong
Yang, Chen
Liang, Dong

المصدر

BioMed Research International

العدد

المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-12، 12ص.

الناشر

Hindawi Publishing Corporation

تاريخ النشر

2020-06-27

دولة النشر

مصر

عدد الصفحات

12

التخصصات الرئيسية

الطب البشري

الملخص EN

Uric acid is the end product of purine metabolism in humans, and its excessive accumulation leads to hyperuricemia and urate crystal deposition in tissues including joints and kidneys.

Hyperuricemia is considered an independent risk factor for cardiovascular and renal diseases.

Although the symptoms of hyperuricemia-induced renal injury have long been known, the pathophysiological molecular mechanisms are not completely understood.

In this review, we focus on the research advances in the mechanisms of hyperuricemia-caused renal injury, primarily on oxidative stress, endothelial dysfunction, renal fibrosis, and inflammation.

Furthermore, we discuss the progress in hyperuricemia management.

نمط استشهاد جمعية علماء النفس الأمريكية (APA)

Su, Hong-yong& Yang, Chen& Liang, Dong& Liu, Hua-feng. 2020. Research Advances in the Mechanisms of Hyperuricemia-Induced Renal Injury. BioMed Research International،Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1134964

نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)

Su, Hong-yong…[et al.]. Research Advances in the Mechanisms of Hyperuricemia-Induced Renal Injury. BioMed Research International No. 2020 (2020), pp.1-12.
https://search.emarefa.net/detail/BIM-1134964

نمط استشهاد الجمعية الطبية الأمريكية (AMA)

Su, Hong-yong& Yang, Chen& Liang, Dong& Liu, Hua-feng. Research Advances in the Mechanisms of Hyperuricemia-Induced Renal Injury. BioMed Research International. 2020. Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1134964

نوع البيانات

مقالات

لغة النص

الإنجليزية

الملاحظات

Includes bibliographical references

رقم السجل

BIM-1134964