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肾脏代谢与高血压。

Renal metabolism and hypertension.

机构信息

The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.

Center of Systems Molecular Medicine, Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA.

出版信息

Nat Commun. 2021 Feb 11;12(1):963. doi: 10.1038/s41467-021-21301-5.

DOI:10.1038/s41467-021-21301-5
PMID:33574248
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7878744/
Abstract

Hypertension is a leading risk factor for disease burden worldwide. The kidneys, which have a high specific metabolic rate, play an essential role in the long-term regulation of arterial blood pressure. In this review, we discuss the emerging role of renal metabolism in the development of hypertension. Renal energy and substrate metabolism is characterized by several important and, in some cases, unique features. Recent advances suggest that alterations of renal metabolism may result from genetic abnormalities or serve initially as a physiological response to environmental stressors to support tubular transport, which may ultimately affect regulatory pathways and lead to unfavorable cellular and pathophysiological consequences that contribute to the development of hypertension.

摘要

高血压是全球疾病负担的主要风险因素。肾脏具有较高的特定代谢率,在长期调节动脉血压方面发挥着重要作用。在这篇综述中,我们讨论了肾脏代谢在高血压发展中的新作用。肾脏的能量和底物代谢具有几个重要的特征,在某些情况下是独特的。最近的进展表明,肾脏代谢的改变可能是由于遗传异常引起的,或者最初是对环境应激的生理反应,以支持肾小管转运,这最终可能影响调节途径,并导致不利的细胞和病理生理后果,从而导致高血压的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6147/7878744/8d217e88890a/41467_2021_21301_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6147/7878744/443ffe426a26/41467_2021_21301_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6147/7878744/b9d21e90495b/41467_2021_21301_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6147/7878744/8d217e88890a/41467_2021_21301_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6147/7878744/443ffe426a26/41467_2021_21301_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6147/7878744/b9d21e90495b/41467_2021_21301_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6147/7878744/8d217e88890a/41467_2021_21301_Fig3_HTML.jpg

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Insufficient fumarase contributes to hypertension by an imbalance of redox metabolism in Dahl salt-sensitive rats.
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Front Pharmacol. 2025 Jun 18;16:1578815. doi: 10.3389/fphar.2025.1578815. eCollection 2025.
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