Mesangial Injury and Capillary Ballooning Precede Podocyte Damage in Nephrosclerosis
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Mesangial Injury and Capillary Ballooning Precede Podocyte Damage in Nephrosclerosis. / Kriz, Wilhelm; Wiech, Thorsten; Gröne, Hermann-Josef.
in: AM J PATHOL, Jahrgang 192, Nr. 12, 12.2022, S. 1670-1682.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Mesangial Injury and Capillary Ballooning Precede Podocyte Damage in Nephrosclerosis
AU - Kriz, Wilhelm
AU - Wiech, Thorsten
AU - Gröne, Hermann-Josef
N1 - Copyright © 2022 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.
PY - 2022/12
Y1 - 2022/12
N2 - The development of focal and segmental glomerulosclerosis (FSGS) as a consequence of glomerular hypertension resulting from arterial hypertension is widely considered a podocyte disease. However, the primary damage is encountered in the mesangium. In acute settings, mesangial cells disconnect from their insertions to the glomerular basement membrane, causing a ballooning of capillaries and severe changes of the folding pattern of the glomerular basement membrane, of the arrangement of the capillaries, and thereby of the architecture of the tuft. The displacement of capillaries led to contact of podocytes and parietal epithelial cells, initiating the formation of tuft adhesions to Bowman's capsule, the committed lesion to progress to FSGS. In addition, the displacement of capillaries also caused an abnormal stretching of podocytes, resulting in podocyte damage. Thus, the podocyte damage that starts the sequence to FSGS is predicted to develop secondary to the mesangial damage. This sequence was found in two hypertensive rat models of FSGS and in human hypertensive nephrosclerosis.
AB - The development of focal and segmental glomerulosclerosis (FSGS) as a consequence of glomerular hypertension resulting from arterial hypertension is widely considered a podocyte disease. However, the primary damage is encountered in the mesangium. In acute settings, mesangial cells disconnect from their insertions to the glomerular basement membrane, causing a ballooning of capillaries and severe changes of the folding pattern of the glomerular basement membrane, of the arrangement of the capillaries, and thereby of the architecture of the tuft. The displacement of capillaries led to contact of podocytes and parietal epithelial cells, initiating the formation of tuft adhesions to Bowman's capsule, the committed lesion to progress to FSGS. In addition, the displacement of capillaries also caused an abnormal stretching of podocytes, resulting in podocyte damage. Thus, the podocyte damage that starts the sequence to FSGS is predicted to develop secondary to the mesangial damage. This sequence was found in two hypertensive rat models of FSGS and in human hypertensive nephrosclerosis.
KW - Rats
KW - Humans
KW - Animals
KW - Podocytes/pathology
KW - Glomerulosclerosis, Focal Segmental/pathology
KW - Nephrosclerosis/complications
KW - Capillaries/pathology
KW - Glomerular Basement Membrane/pathology
KW - Hypertension, Renal/complications
U2 - 10.1016/j.ajpath.2022.08.007
DO - 10.1016/j.ajpath.2022.08.007
M3 - SCORING: Journal article
C2 - 36150506
VL - 192
SP - 1670
EP - 1682
JO - AM J PATHOL
JF - AM J PATHOL
SN - 0002-9440
IS - 12
ER -