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Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways
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| Zeitschriftentitel: | Physiological Genomics |
|---|---|
| Personen und Körperschaften: | , , , , , |
| In: | Physiological Genomics, 45, 2013, 16, S. 710-719 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
|
| Schlagwörter: |
| author_facet |
Kelly, K. J. Liu, Yunlong Zhang, Jizhong Goswami, Chirayu Lin, Hai Dominguez, Jesus H. Kelly, K. J. Liu, Yunlong Zhang, Jizhong Goswami, Chirayu Lin, Hai Dominguez, Jesus H. |
|---|---|
| author |
Kelly, K. J. Liu, Yunlong Zhang, Jizhong Goswami, Chirayu Lin, Hai Dominguez, Jesus H. |
| spellingShingle |
Kelly, K. J. Liu, Yunlong Zhang, Jizhong Goswami, Chirayu Lin, Hai Dominguez, Jesus H. Physiological Genomics Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways Genetics Physiology |
| author_sort |
kelly, k. j. |
| spelling |
Kelly, K. J. Liu, Yunlong Zhang, Jizhong Goswami, Chirayu Lin, Hai Dominguez, Jesus H. 1094-8341 1531-2267 American Physiological Society Genetics Physiology http://dx.doi.org/10.1152/physiolgenomics.00028.2013 <jats:p> Despite advances in the treatment of diabetic nephropathy (DN), currently available therapies have not prevented the epidemic of progressive chronic kidney disease (CKD). The morbidity of CKD, and the inexorable increase in the prevalence of end-stage renal disease, demands more effective approaches to prevent and treat progressive CKD. We undertook next-generation sequencing in a rat model of diabetic nephropathy to study in depth the pathogenic alterations involved in DN with progressive CKD. We employed the obese, diabetic ZS rat, a model that develops diabetic nephropathy, characterized by progressive CKD, inflammation, and fibrosis, the hallmarks of human disease. We then used RNA-seq to examine the combined effects of renal cells and infiltrating inflammatory cells acting as a pathophysiological unit. The comprehensive systems biology analysis of progressive CKD revealed multiple interactions of altered genes that were integrated into morbid networks. These pathological gene assemblies lead to renal inflammation and promote apoptosis and cell cycle arrest in progressive CKD. Moreover, in what is clearly a major therapeutic challenge, multiple and redundant pathways were found to be linked to renal fibrosis, a major cause of kidney loss. We conclude that systems biology applied to progressive CKD in DN can be used to develop novel therapeutic strategies directed to restore critical anomalies in affected gene networks. </jats:p> Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways Physiological Genomics |
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| title |
Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways |
| title_unstemmed |
Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways |
| title_full |
Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways |
| title_fullStr |
Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways |
| title_full_unstemmed |
Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways |
| title_short |
Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways |
| title_sort |
comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways |
| topic |
Genetics Physiology |
| url |
http://dx.doi.org/10.1152/physiolgenomics.00028.2013 |
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2013 |
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710-719 |
| description |
<jats:p> Despite advances in the treatment of diabetic nephropathy (DN), currently available therapies have not prevented the epidemic of progressive chronic kidney disease (CKD). The morbidity of CKD, and the inexorable increase in the prevalence of end-stage renal disease, demands more effective approaches to prevent and treat progressive CKD. We undertook next-generation sequencing in a rat model of diabetic nephropathy to study in depth the pathogenic alterations involved in DN with progressive CKD. We employed the obese, diabetic ZS rat, a model that develops diabetic nephropathy, characterized by progressive CKD, inflammation, and fibrosis, the hallmarks of human disease. We then used RNA-seq to examine the combined effects of renal cells and infiltrating inflammatory cells acting as a pathophysiological unit. The comprehensive systems biology analysis of progressive CKD revealed multiple interactions of altered genes that were integrated into morbid networks. These pathological gene assemblies lead to renal inflammation and promote apoptosis and cell cycle arrest in progressive CKD. Moreover, in what is clearly a major therapeutic challenge, multiple and redundant pathways were found to be linked to renal fibrosis, a major cause of kidney loss. We conclude that systems biology applied to progressive CKD in DN can be used to develop novel therapeutic strategies directed to restore critical anomalies in affected gene networks. </jats:p> |
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| author | Kelly, K. J., Liu, Yunlong, Zhang, Jizhong, Goswami, Chirayu, Lin, Hai, Dominguez, Jesus H. |
| author_facet | Kelly, K. J., Liu, Yunlong, Zhang, Jizhong, Goswami, Chirayu, Lin, Hai, Dominguez, Jesus H., Kelly, K. J., Liu, Yunlong, Zhang, Jizhong, Goswami, Chirayu, Lin, Hai, Dominguez, Jesus H. |
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| description | <jats:p> Despite advances in the treatment of diabetic nephropathy (DN), currently available therapies have not prevented the epidemic of progressive chronic kidney disease (CKD). The morbidity of CKD, and the inexorable increase in the prevalence of end-stage renal disease, demands more effective approaches to prevent and treat progressive CKD. We undertook next-generation sequencing in a rat model of diabetic nephropathy to study in depth the pathogenic alterations involved in DN with progressive CKD. We employed the obese, diabetic ZS rat, a model that develops diabetic nephropathy, characterized by progressive CKD, inflammation, and fibrosis, the hallmarks of human disease. We then used RNA-seq to examine the combined effects of renal cells and infiltrating inflammatory cells acting as a pathophysiological unit. The comprehensive systems biology analysis of progressive CKD revealed multiple interactions of altered genes that were integrated into morbid networks. These pathological gene assemblies lead to renal inflammation and promote apoptosis and cell cycle arrest in progressive CKD. Moreover, in what is clearly a major therapeutic challenge, multiple and redundant pathways were found to be linked to renal fibrosis, a major cause of kidney loss. We conclude that systems biology applied to progressive CKD in DN can be used to develop novel therapeutic strategies directed to restore critical anomalies in affected gene networks. </jats:p> |
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| spelling | Kelly, K. J. Liu, Yunlong Zhang, Jizhong Goswami, Chirayu Lin, Hai Dominguez, Jesus H. 1094-8341 1531-2267 American Physiological Society Genetics Physiology http://dx.doi.org/10.1152/physiolgenomics.00028.2013 <jats:p> Despite advances in the treatment of diabetic nephropathy (DN), currently available therapies have not prevented the epidemic of progressive chronic kidney disease (CKD). The morbidity of CKD, and the inexorable increase in the prevalence of end-stage renal disease, demands more effective approaches to prevent and treat progressive CKD. We undertook next-generation sequencing in a rat model of diabetic nephropathy to study in depth the pathogenic alterations involved in DN with progressive CKD. We employed the obese, diabetic ZS rat, a model that develops diabetic nephropathy, characterized by progressive CKD, inflammation, and fibrosis, the hallmarks of human disease. We then used RNA-seq to examine the combined effects of renal cells and infiltrating inflammatory cells acting as a pathophysiological unit. The comprehensive systems biology analysis of progressive CKD revealed multiple interactions of altered genes that were integrated into morbid networks. These pathological gene assemblies lead to renal inflammation and promote apoptosis and cell cycle arrest in progressive CKD. Moreover, in what is clearly a major therapeutic challenge, multiple and redundant pathways were found to be linked to renal fibrosis, a major cause of kidney loss. We conclude that systems biology applied to progressive CKD in DN can be used to develop novel therapeutic strategies directed to restore critical anomalies in affected gene networks. </jats:p> Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways Physiological Genomics |
| spellingShingle | Kelly, K. J., Liu, Yunlong, Zhang, Jizhong, Goswami, Chirayu, Lin, Hai, Dominguez, Jesus H., Physiological Genomics, Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways, Genetics, Physiology |
| title | Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways |
| title_full | Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways |
| title_fullStr | Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways |
| title_full_unstemmed | Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways |
| title_short | Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways |
| title_sort | comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways |
| title_unstemmed | Comprehensive genomic profiling in diabetic nephropathy reveals the predominance of proinflammatory pathways |
| topic | Genetics, Physiology |
| url | http://dx.doi.org/10.1152/physiolgenomics.00028.2013 |