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J. Clin. Med. 2018, 7(8), 225; https://doi.org/10.3390/jcm7080225

The Emerging Role of Pathogenesis of IgA Nephropathy

1
Department of Emergency Medicine, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei City 231, Taiwan
2
Department of Emergency Medicine, School of Medicine, Tzu Chi University, Hualien 970, Taiwan
3
Yuh-Ing Junior College of Health Care & Management, Kaohsiung 807, Taiwan
4
Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung 813, Taiwan
5
Department of Obstetrics and Gynecology, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei City 231, Taiwan
6
Department of Obstetrics and Gynecology, School of Medicine, Tzu Chi University, Hualien 970, Taiwan
7
Division of Nephrology, Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine National Cheng Kung University, Tainan 704, Taiwan
8
Division of Nephrology, Department of Internal Medicine, Chang Bing Show Chwan Memorial Hospital, Changhua 505, Taiwan
9
Research Assistant Center, Show Chwan Memorial Hospital, Changhua 500, Taiwan
These authors contributed equally to the research.
*
Authors to whom correspondence should be addressed.
Received: 28 July 2018 / Revised: 12 August 2018 / Accepted: 16 August 2018 / Published: 20 August 2018
(This article belongs to the Section Nephrology & Urology)
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Abstract

IgA nephropathy is an autoimmune disease induced by fthe ormation of galactose-deficient IgA1 and anti-glycans autoantibody. A multi-hit hypothesis was promoted to explain full expression of IgA nephropathy. The deposition of immune complex resulted in activation of the complement, increasing oxidative stress, promoting inflammatory cascade, and inducing cell apoptosis via mesangio-podocytic-tubular crosstalk. The interlinked signaling pathways of immune-complex-mediated inflammation can offer a novel target for therapeutic approaches. Treatments of IgA nephropathy are also summarized in our review article. In this article, we provide an overview of the recent basic and clinical studies in cell molecular regulation of IgAN for further treatment interventions. View Full-Text
Keywords: inflammation; IgA nephropathy; anti-glycans autoantibody; galactose-deficient IgA1; mesangio-podocytic-tubular crosstalk inflammation; IgA nephropathy; anti-glycans autoantibody; galactose-deficient IgA1; mesangio-podocytic-tubular crosstalk
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Wu, M.-Y.; Chen, C.-S.; Yiang, G.-T.; Cheng, P.-W.; Chen, Y.-L.; Chiu, H.-C.; Liu, K.-H.; Lee, W.-C.; Li, C.-J. The Emerging Role of Pathogenesis of IgA Nephropathy. J. Clin. Med. 2018, 7, 225.

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