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Int J Mol Sci. 2019 Apr 30;20(9). pii: E2138. doi: 10.3390/ijms20092138.

Molecular Mechanisms of Kidney Injury and Repair in Arterial Hypertension.

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Department of Nephrology and Medical Intensive Care, Charité-Universitätsmedizin Berlin, 13353 Berlin, Germany.
Max-Delbrück Center for Molecular Medicine in the Helmholtz Association, 13125 Berlin, Germany.
Experimental and Clinical Research Center, a joint cooperation of Max-Delbrück Center for Molecular Medicine and Charité-Universitätsmedizin Berlin, 13125 Berlin, Germany.
Berlin Institute of Health (BIH), 10178 Berlin, Germany.
Department of Nephrology and Medical Intensive Care, Charité-Universitätsmedizin Berlin, 13353 Berlin, Germany.


The global burden of chronic kidney disease is rising. The etiologies, heterogeneous, and arterial hypertension, are key factors contributing to the development and progression of chronic kidney disease. Arterial hypertension is induced and maintained by a complex network of systemic signaling pathways, such as the hormonal axis of the renin-angiotensin-aldosterone system, hemodynamic alterations affecting blood flow, oxygen supply, and the immune system. This review summarizes the clinical and histopathological features of hypertensive kidney injury and focusses on the interplay of distinct systemic signaling pathways, which drive hypertensive kidney injury in distinct cell types of the kidney. There are several parallels between hypertension-induced molecular signaling cascades in the renal epithelial, endothelial, interstitial, and immune cells. Angiotensin II signaling via the AT1R, hypoxia induced HIFα activation and mechanotransduction are closely interacting and further triggering the adaptions of metabolism, cytoskeletal rearrangement, and profibrotic TGF signaling. The interplay of these, and other cellular pathways, is crucial to balancing the injury and repair of the kidneys and determines the progression of hypertensive kidney disease.


hypertension; kidney; molecular signaling

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