Purpose of review: This review focuses on the role of the mitochondrial protein induced in high glucose 1 (IHG-1) in kidney fibrosis.
Recent findings: Diabetic nephropathy is the most common cause of end-stage renal disease. Transforming growth factor-β1 (TGF-β1) is a pivotal mediator of fibrosis and diabetic nephropathy. IHG-1 was identified in a screen for genes differentially expressed in renal cells exposed to high glucose. Here we review the biology of this novel functionally uncharacterized gene transcript. Data from human biopsy material and experimental models indicate increased expression of IHG-1 is a critical component of fibrogenesis as it amplifies TGF-β1 signalling. IHG-1 is expressed in mitochondria, stabilizes PGC-1α protein and increases mitochondrial biogenesis. Recently the crystal structure of IHG-1 has been determined revealing structural homology with canonical 5'→ 3' DNA polymerases and adenylyl/guanylyl cyclases, whereas the closely related yeast homologue has been shown to function as a tRNA(HIS) guanyltransferase.
Summary: IHG-1 is a transcript up-regulated in renal cells exposed to high glucose, in animal models of renal fibrosis and in human diabetic nephropathy. IHG-1 encodes a mitochondrial protein that amplifies fibrotic responses to TGF-β1 and promotes mitochondrial biogenesis. Investigation of the functional significance of the highly conserved domains of IHG-1 may lead to new therapeutic strategies.
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| Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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| Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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| Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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| Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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| Site | Modification | Modifier | Source | Reference |
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| Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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| Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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| Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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| Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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