Ectodomain shedding by ADAM proteases as a central regulator in kidney physiology and disease

Catherine Meyer-Schwesinger; Lisa Seipold; Paul Saftig

doi:10.1016/j.bbamcr.2021.119165

Ectodomain shedding by ADAM proteases as a central regulator in kidney physiology and disease

Standard

Ectodomain shedding by ADAM proteases as a central regulator in kidney physiology and disease. / Meyer-Schwesinger, Catherine; Seipold, Lisa; Saftig, Paul.

In: BBA-MOL CELL RES, Vol. 1869, No. 3, 119165, 03.2022.

Research output: SCORING: Contribution to journal › SCORING: Review article › Research

Harvard

Meyer-Schwesinger, C, Seipold, L & Saftig, P 2022, 'Ectodomain shedding by ADAM proteases as a central regulator in kidney physiology and disease', BBA-MOL CELL RES, vol. 1869, no. 3, 119165. https://doi.org/10.1016/j.bbamcr.2021.119165

APA

Meyer-Schwesinger, C., Seipold, L., & Saftig, P. (2022). Ectodomain shedding by ADAM proteases as a central regulator in kidney physiology and disease. BBA-MOL CELL RES, 1869(3), [119165]. https://doi.org/10.1016/j.bbamcr.2021.119165

Vancouver

Meyer-Schwesinger C, Seipold L, Saftig P. Ectodomain shedding by ADAM proteases as a central regulator in kidney physiology and disease. BBA-MOL CELL RES. 2022 Mar;1869(3). 119165. https://doi.org/10.1016/j.bbamcr.2021.119165

Bibtex

@article{9b50100841d74e51910c7e4e52331530,

title = "Ectodomain shedding by ADAM proteases as a central regulator in kidney physiology and disease",

abstract = "Besides its involvement in blood and bone physiology, the kidney's main function is to filter substances and thereby regulate the electrolyte composition of body fluids, acid-base balance and toxin removal. Depending on underlying conditions, the nephron must undergo remodeling and cellular adaptations. The proteolytic removal of cell surface proteins via ectodomain shedding by A Disintegrin and Metalloproteases (ADAMs) is of importance for the regulation of cell-cell and cell-matrix adhesion of renal cells. ADAM10 controls glomerular and tubule development in a Notch1 signaling-dependent manner and regulates brush border composition. ADAM17 regulates the renin angiotensin system and is together with ADAM10 involved in calcium phosphate homeostasis. In kidney disease ADAMs, especially ADAM17 contribute to inflammation through their involvement in IL-6 trans-signaling, Notch-, epithelial growth factor receptor-, and tumor necrosis factor α signaling. ADAMs are interesting drug targets to reduce the inflammatory burden, defective cell adhesion and impaired signaling pathways in kidney diseases.",

author = "Catherine Meyer-Schwesinger and Lisa Seipold and Paul Saftig",

year = "2022",

month = mar,

doi = "10.1016/j.bbamcr.2021.119165",

language = "English",

volume = "1869",

journal = "BBA-MOL CELL RES",

issn = "0167-4889",

publisher = "Elsevier",

number = "3",

}

RIS

TY - JOUR

T1 - Ectodomain shedding by ADAM proteases as a central regulator in kidney physiology and disease

AU - Meyer-Schwesinger, Catherine

AU - Seipold, Lisa

AU - Saftig, Paul

PY - 2022/3

Y1 - 2022/3

N2 - Besides its involvement in blood and bone physiology, the kidney's main function is to filter substances and thereby regulate the electrolyte composition of body fluids, acid-base balance and toxin removal. Depending on underlying conditions, the nephron must undergo remodeling and cellular adaptations. The proteolytic removal of cell surface proteins via ectodomain shedding by A Disintegrin and Metalloproteases (ADAMs) is of importance for the regulation of cell-cell and cell-matrix adhesion of renal cells. ADAM10 controls glomerular and tubule development in a Notch1 signaling-dependent manner and regulates brush border composition. ADAM17 regulates the renin angiotensin system and is together with ADAM10 involved in calcium phosphate homeostasis. In kidney disease ADAMs, especially ADAM17 contribute to inflammation through their involvement in IL-6 trans-signaling, Notch-, epithelial growth factor receptor-, and tumor necrosis factor α signaling. ADAMs are interesting drug targets to reduce the inflammatory burden, defective cell adhesion and impaired signaling pathways in kidney diseases.

AB - Besides its involvement in blood and bone physiology, the kidney's main function is to filter substances and thereby regulate the electrolyte composition of body fluids, acid-base balance and toxin removal. Depending on underlying conditions, the nephron must undergo remodeling and cellular adaptations. The proteolytic removal of cell surface proteins via ectodomain shedding by A Disintegrin and Metalloproteases (ADAMs) is of importance for the regulation of cell-cell and cell-matrix adhesion of renal cells. ADAM10 controls glomerular and tubule development in a Notch1 signaling-dependent manner and regulates brush border composition. ADAM17 regulates the renin angiotensin system and is together with ADAM10 involved in calcium phosphate homeostasis. In kidney disease ADAMs, especially ADAM17 contribute to inflammation through their involvement in IL-6 trans-signaling, Notch-, epithelial growth factor receptor-, and tumor necrosis factor α signaling. ADAMs are interesting drug targets to reduce the inflammatory burden, defective cell adhesion and impaired signaling pathways in kidney diseases.

U2 - 10.1016/j.bbamcr.2021.119165

DO - 10.1016/j.bbamcr.2021.119165

M3 - SCORING: Review article

C2 - 34699872

VL - 1869

JO - BBA-MOL CELL RES

JF - BBA-MOL CELL RES

SN - 0167-4889

IS - 3

M1 - 119165

ER -