Molecular Biology of IgA Nephropathy
A special issue of Journal of Clinical Medicine (ISSN 2077-0383).
Deadline for manuscript submissions: closed (31 March 2017)
Special Issue Editors
Interests: genetics of autism; neural tube defects; familial hemiplegia; genetics of complex diseases; epigenetics of colon cancer; genetics of kidney diseases
Interests: mouse genetics; embryological development; molecular bases of cancer; genetics of familial kidney diseases
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
IgA nephropathy represents a mysterious disease from many aspects. It is one of the most common primary glomerulopathies worldwide, with a strong genetic basis, but no single gene has been firmly found to be mutated in most of the sporadic or familial cases. Several good studies, using GWAS and linkage analysis, have highlighted the role of different variants in different genes, but no one clear pathway has clearly emerged. In the pathogenesis of the disease, a prominent role has been attributed to the hypogalactosylation of IgA, but neither the genetic nor the enzymatic cause of this defect have been established. Hypogalactosylation itself cannot be used, alone, as a biomarker of the disease to establish a diagnosis or to follow up the evolution of the renal damage. It is not clear whether IgA nephropathy represents an autoimmune condition rather than a disease, where a dysregulated immune system plays a central role. These uncertainties mirror the difficulties in the medical treatment and, thus far, no clear treatment has been found to be able to substantially modify the course of the disease. Please join us in presenting this Special Issue on the state-of-the-art research currently being performed worldwide on IgA nephropathy to help to establish future research directions to help clarify genetic causes, pathogenesis and new targeted therapies.
Dr. Fiorella Gurrier
Dr. Eugenio Sangiorgi
Guest Editors
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Keywords
- IgA nephropathy
- immune system
- defective galactosylation
- complex diseases
- GWAS studies
- genetics
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