Mechanisms of Scarring in Focal Segmental Glomerulosclerosis

被引：14

作者：

Zhong, Jianyong ^{[1
,2
]}

Whitman, Jacob B. ^{[1
]}

Yang, Hai-Chun ^{[1
,2
]}

Fogo, Agnes B. ^{[1
,2
]}

机构：

[1] Vanderbilt Univ, Med Ctr, Dept Pathol Microbiol & Immunol, MCN C3310, Nashville, TN 37232 USA

[2] Vanderbilt Univ, Med Ctr, Div Pediat Nephrol, Nashville, TN USA

来源：

JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY | 2019年 / 67卷 / 09期

关键词：

chronic kidney disease; endothelial cell; extracellular matrix; fibrosis; FSGS; parietal epithelial cell; podocyte; transforming growth factor beta; tubular epithelial cell; PARIETAL EPITHELIAL-CELLS; SOLUBLE UROKINASE RECEPTOR; PROXIMAL TUBULAR INJURY; PODOCYTE INJURY; PLASMINOGEN-ACTIVATOR; ATUBULAR GLOMERULI; DOWN-REGULATION; KIDNEY-DISEASE; REGENERATION; EXPRESSION;

D O I：

10.1369/0022155419850170

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Focal segmental glomerulosclerosis (FSGS) presents with scar in parts of some glomeruli and often progresses to global and diffuse glomerulosclerosis. Podocyte injury is the initial target in primary FSGS, induced by a circulating factor. Several gene variants, for example, APOL1, are associated with increased susceptibility to FSGS. Primary FSGS may be due to genetic mutation in key podocyte genes. Increased work stress after loss of nephrons, epigenetic mechanisms, and various profibrotic pathways can contribute to progressive sclerosis, regardless of the initial injury. The progression of FSGS lesions also involves crosstalk between podocytes and other kidney cells, such as parietal epithelial cells, glomerular endothelial cells, and even tubular epithelial cells. New insights related to these mechanisms could potentially lead to new therapeutic strategies to prevent progression of FSGS.

引用

页码：623 / 632

页数：10

共 83 条

[1] The phenotypes of podocytes and parietal epithelial cells may overlap in diabetic nephropathy [J].

Andeen, Nicole K. ;

Nguyen, Tri Q. ;

Steegh, Floor ;

Hudkins, Kelly L. ;

Najafian, Behzad ;

Alpers, Charles E. .

KIDNEY INTERNATIONAL, 2015, 88 (05) :1099-1107

[2] Transgenic expression of human APOL1 risk variants in podocytes induces kidney disease in mice [J].

Beckerman, Pazit ;

Bi-Karchin, Jing ;

Park, Ae Seo Deok ;

Qiu, Chengxiang ;

Dummer, Patrick D. ;

Soomro, Irfana ;

Boustany-Kari, Carine M. ;

Pullen, Steven S. ;

Miner, Jeffrey H. ;

Hu, Chien-An A. ;

Rohacs, Tibor ;

Inoue, Kazunori ;

Ishibe, Shuta ;

Saleem, Moin A. ;

Palmer, Matthew B. ;

Cuervo, Ana Maria ;

Kopp, Jeffrey B. ;

Susztak, Katalin .

NATURE MEDICINE, 2017, 23 (04) :429-+

[3] The Regenerative Potential of Parietal Epithelial Cells in Adult Mice [J].

Berger, Katja ;

Schulte, Kevin ;

Boor, Peter ;

Kuppe, Christoph ;

van Kuppevelt, Toin H. ;

Floege, Juergen ;

Smeets, Bart ;

Moeller, Marcus J. .

JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2014, 25 (04) :693-705

[4] Focal Segmental Glomerulosclerosis [J].

D'Agati, Vivette D. ;

Kaskel, Frederick J. ;

Falk, Ronald J. .

NEW ENGLAND JOURNAL OF MEDICINE, 2011, 365 (25) :2398-2411

[5] Endothelial mitochondrial oxidative stress determines podocyte depletion in segmental glomerulosclerosis [J].

Daehn, Ilse ;

Casalena, Gabriella ;

Zhang, Taoran ;

Shi, Shaolin ;

Fenninger, Franz ;

Barasch, Nicholas ;

Yu, Liping ;

D'Agati, Vivette ;

Schlondorff, Detlef ;

Kriz, Wilhelm ;

Haraldsson, Borje ;

Bottinger, Erwin P. .

JOURNAL OF CLINICAL INVESTIGATION, 2014, 124 (04) :1608-1621

[6] A circulating antibody panel for pretransplant prediction of FSGS recurrence after kidney transplantation [J].

Delville, Marianne ;

Sigdel, Tara K. ;

Wei, Changli ;

Li, Jing ;

Hsieh, Szu-Chuan ;

Fornoni, Alessia ;

Burke, George W. ;

Bruneval, Patrick ;

Naesens, Maarten ;

Jackson, Annette ;

Alachkar, Nada ;

Canaud, Guillaume ;

Legendre, Christophe ;

Anglicheau, Dany ;

Reiser, Jochen ;

Sarwal, Minnie M. .

SCIENCE TRANSLATIONAL MEDICINE, 2014, 6 (256)

[7] Glomerular parietal epithelial cells contribute to adult podocyte regeneration in experimental focal segmental glomerulosclerosis [J].

Eng, Diana G. ;

Sunseri, Maria W. ;

Kaverina, Natalya V. ;

Roeder, Sebastian S. ;

Pippin, Jeffrey W. ;

Shankland, Stuart J. .

KIDNEY INTERNATIONAL, 2015, 88 (05) :999-1012

[8] Glomerular-specific alterations of VEGF-A expression lead to distinct congenital and acquired renal diseases [J].

Eremina, V ;

Sood, M ;

Haigh, J ;

Nagy, A ;

Lajoie, G ;

Ferrara, N ;

Gerber, HP ;

Kikkawa, Y ;

Miner, JH ;

Quaggin, SE .

JOURNAL OF CLINICAL INVESTIGATION, 2003, 111 (05) :707-716

[9] VEGF inhibition and renal thrombotic microangiopathy [J].

Eremina, Vera ;

Jefferson, J. Ashley ;

Kowalewska, Jolanta ;

Hochster, Howard ;

Haas, Mark ;

Weisstuch, Joseph ;

Richardson, Catherine ;

Kopp, Jeffrey B. ;

Kabir, M. Golam ;

Backx, Peter H. ;

Gerber, Hans-Peter ;

Ferrara, Napoleone ;

Barisoni, Laura ;

Alpers, Charles E. ;

Quaggin, Susan E. .

NEW ENGLAND JOURNAL OF MEDICINE, 2008, 358 (11) :1129-1136

[10] Parietal Epithelial Cell Activation Marker in Early Recurrence of FSGS in the Transplant [J].

Fatima, Huma ;

Moeller, Marcus J. ;

Smeets, Bart ;

Yang, Hai-Chun ;

D'Agati, Vivette D. ;

Alpers, Charles E. ;

Fogo, Agnes B. .

CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2012, 7 (11) :1852-1858

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