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Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy?
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| Zeitschriftentitel: | British Journal of Pharmacology |
|---|---|
| Personen und Körperschaften: | , |
| In: | British Journal of Pharmacology, 171, 2014, 8, S. 1917-1942 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
|
| Schlagwörter: |
| author_facet |
Higgins, G C Coughlan, M T Higgins, G C Coughlan, M T |
|---|---|
| author |
Higgins, G C Coughlan, M T |
| spellingShingle |
Higgins, G C Coughlan, M T British Journal of Pharmacology Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? Pharmacology |
| author_sort |
higgins, g c |
| spelling |
Higgins, G C Coughlan, M T 0007-1188 1476-5381 Wiley Pharmacology http://dx.doi.org/10.1111/bph.12503 <jats:sec><jats:label /><jats:p>Diabetic nephropathy (<jats:styled-content style="fixed-case">DN</jats:styled-content>) is a progressive microvascular complication arising from diabetes. Within the kidney, the glomeruli, tubules, vessels and interstitium are disrupted, ultimately impairing renal function and leading to end‐stage renal disease (<jats:styled-content style="fixed-case">ESRD</jats:styled-content>). Current pharmacological therapies used in individuals with <jats:styled-content style="fixed-case">DN</jats:styled-content> do not prevent the inevitable progression to <jats:styled-content style="fixed-case">ESRD</jats:styled-content>; therefore, new targets of therapy are urgently required. Studies from animal models indicate that disturbances in mitochondrial homeostasis are central to the pathogenesis of <jats:styled-content style="fixed-case">DN</jats:styled-content>. Since renal proximal tubule cells rely on oxidative phosphorylation to provide adequate <jats:styled-content style="fixed-case">ATP</jats:styled-content> for tubular reabsorption, an impairment of mitochondrial bioenergetics can result in renal functional decline. Defects at the level of the electron transport chain have long been established in <jats:styled-content style="fixed-case">DN</jats:styled-content>, promoting electron leakage and formation of superoxide radicals, mediating microinflammation and contributing to the renal lesion. More recent studies suggest that mitochondrial‐associated proteins may be directly involved in the pathogenesis of tubulointerstitial fibrosis and glomerulosclerosis. An accumulation of fragmented mitochondria are found in the renal cortex in both humans and animals with <jats:styled-content style="fixed-case">DN</jats:styled-content>, suggesting that in tandem with a shift in dynamics, mitochondrial clearance mechanisms may be impaired. The process of mitophagy is the selective targeting of damaged or dysfunctional mitochondria to autophagosomes for degradation through the autophagy pathway. The current review explores the concept that an impairment in the mitophagy system leads to the accelerated progression of renal pathology. A better understanding of the cellular and molecular events that govern mitophagy and dynamics in <jats:styled-content style="fixed-case">DN</jats:styled-content> may lead to improved therapeutic strategies.</jats:p></jats:sec><jats:sec><jats:title>Linked Articles</jats:title><jats:p>This article is part of a themed issue on Mitochondrial Pharmacology: Energy, Injury & Beyond. To view the other articles in this issue visit <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="http://dx.doi.org/10.1111/bph.2014.171.issue-8">http://dx.doi.org/10.1111/bph.2014.171.issue‐8</jats:ext-link></jats:p></jats:sec> Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? British Journal of Pharmacology |
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2014 |
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| title |
Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? |
| title_unstemmed |
Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? |
| title_full |
Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? |
| title_fullStr |
Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? |
| title_full_unstemmed |
Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? |
| title_short |
Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? |
| title_sort |
mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? |
| topic |
Pharmacology |
| url |
http://dx.doi.org/10.1111/bph.12503 |
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2014 |
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1917-1942 |
| description |
<jats:sec><jats:label /><jats:p>Diabetic nephropathy (<jats:styled-content style="fixed-case">DN</jats:styled-content>) is a progressive microvascular complication arising from diabetes. Within the kidney, the glomeruli, tubules, vessels and interstitium are disrupted, ultimately impairing renal function and leading to end‐stage renal disease (<jats:styled-content style="fixed-case">ESRD</jats:styled-content>). Current pharmacological therapies used in individuals with <jats:styled-content style="fixed-case">DN</jats:styled-content> do not prevent the inevitable progression to <jats:styled-content style="fixed-case">ESRD</jats:styled-content>; therefore, new targets of therapy are urgently required. Studies from animal models indicate that disturbances in mitochondrial homeostasis are central to the pathogenesis of <jats:styled-content style="fixed-case">DN</jats:styled-content>. Since renal proximal tubule cells rely on oxidative phosphorylation to provide adequate <jats:styled-content style="fixed-case">ATP</jats:styled-content> for tubular reabsorption, an impairment of mitochondrial bioenergetics can result in renal functional decline. Defects at the level of the electron transport chain have long been established in <jats:styled-content style="fixed-case">DN</jats:styled-content>, promoting electron leakage and formation of superoxide radicals, mediating microinflammation and contributing to the renal lesion. More recent studies suggest that mitochondrial‐associated proteins may be directly involved in the pathogenesis of tubulointerstitial fibrosis and glomerulosclerosis. An accumulation of fragmented mitochondria are found in the renal cortex in both humans and animals with <jats:styled-content style="fixed-case">DN</jats:styled-content>, suggesting that in tandem with a shift in dynamics, mitochondrial clearance mechanisms may be impaired. The process of mitophagy is the selective targeting of damaged or dysfunctional mitochondria to autophagosomes for degradation through the autophagy pathway. The current review explores the concept that an impairment in the mitophagy system leads to the accelerated progression of renal pathology. A better understanding of the cellular and molecular events that govern mitophagy and dynamics in <jats:styled-content style="fixed-case">DN</jats:styled-content> may lead to improved therapeutic strategies.</jats:p></jats:sec><jats:sec><jats:title>Linked Articles</jats:title><jats:p>This article is part of a themed issue on Mitochondrial Pharmacology: Energy, Injury & Beyond. To view the other articles in this issue visit <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="http://dx.doi.org/10.1111/bph.2014.171.issue-8">http://dx.doi.org/10.1111/bph.2014.171.issue‐8</jats:ext-link></jats:p></jats:sec> |
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| description | <jats:sec><jats:label /><jats:p>Diabetic nephropathy (<jats:styled-content style="fixed-case">DN</jats:styled-content>) is a progressive microvascular complication arising from diabetes. Within the kidney, the glomeruli, tubules, vessels and interstitium are disrupted, ultimately impairing renal function and leading to end‐stage renal disease (<jats:styled-content style="fixed-case">ESRD</jats:styled-content>). Current pharmacological therapies used in individuals with <jats:styled-content style="fixed-case">DN</jats:styled-content> do not prevent the inevitable progression to <jats:styled-content style="fixed-case">ESRD</jats:styled-content>; therefore, new targets of therapy are urgently required. Studies from animal models indicate that disturbances in mitochondrial homeostasis are central to the pathogenesis of <jats:styled-content style="fixed-case">DN</jats:styled-content>. Since renal proximal tubule cells rely on oxidative phosphorylation to provide adequate <jats:styled-content style="fixed-case">ATP</jats:styled-content> for tubular reabsorption, an impairment of mitochondrial bioenergetics can result in renal functional decline. Defects at the level of the electron transport chain have long been established in <jats:styled-content style="fixed-case">DN</jats:styled-content>, promoting electron leakage and formation of superoxide radicals, mediating microinflammation and contributing to the renal lesion. More recent studies suggest that mitochondrial‐associated proteins may be directly involved in the pathogenesis of tubulointerstitial fibrosis and glomerulosclerosis. An accumulation of fragmented mitochondria are found in the renal cortex in both humans and animals with <jats:styled-content style="fixed-case">DN</jats:styled-content>, suggesting that in tandem with a shift in dynamics, mitochondrial clearance mechanisms may be impaired. The process of mitophagy is the selective targeting of damaged or dysfunctional mitochondria to autophagosomes for degradation through the autophagy pathway. The current review explores the concept that an impairment in the mitophagy system leads to the accelerated progression of renal pathology. A better understanding of the cellular and molecular events that govern mitophagy and dynamics in <jats:styled-content style="fixed-case">DN</jats:styled-content> may lead to improved therapeutic strategies.</jats:p></jats:sec><jats:sec><jats:title>Linked Articles</jats:title><jats:p>This article is part of a themed issue on Mitochondrial Pharmacology: Energy, Injury & Beyond. To view the other articles in this issue visit <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="http://dx.doi.org/10.1111/bph.2014.171.issue-8">http://dx.doi.org/10.1111/bph.2014.171.issue‐8</jats:ext-link></jats:p></jats:sec> |
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| spelling | Higgins, G C Coughlan, M T 0007-1188 1476-5381 Wiley Pharmacology http://dx.doi.org/10.1111/bph.12503 <jats:sec><jats:label /><jats:p>Diabetic nephropathy (<jats:styled-content style="fixed-case">DN</jats:styled-content>) is a progressive microvascular complication arising from diabetes. Within the kidney, the glomeruli, tubules, vessels and interstitium are disrupted, ultimately impairing renal function and leading to end‐stage renal disease (<jats:styled-content style="fixed-case">ESRD</jats:styled-content>). Current pharmacological therapies used in individuals with <jats:styled-content style="fixed-case">DN</jats:styled-content> do not prevent the inevitable progression to <jats:styled-content style="fixed-case">ESRD</jats:styled-content>; therefore, new targets of therapy are urgently required. Studies from animal models indicate that disturbances in mitochondrial homeostasis are central to the pathogenesis of <jats:styled-content style="fixed-case">DN</jats:styled-content>. Since renal proximal tubule cells rely on oxidative phosphorylation to provide adequate <jats:styled-content style="fixed-case">ATP</jats:styled-content> for tubular reabsorption, an impairment of mitochondrial bioenergetics can result in renal functional decline. Defects at the level of the electron transport chain have long been established in <jats:styled-content style="fixed-case">DN</jats:styled-content>, promoting electron leakage and formation of superoxide radicals, mediating microinflammation and contributing to the renal lesion. More recent studies suggest that mitochondrial‐associated proteins may be directly involved in the pathogenesis of tubulointerstitial fibrosis and glomerulosclerosis. An accumulation of fragmented mitochondria are found in the renal cortex in both humans and animals with <jats:styled-content style="fixed-case">DN</jats:styled-content>, suggesting that in tandem with a shift in dynamics, mitochondrial clearance mechanisms may be impaired. The process of mitophagy is the selective targeting of damaged or dysfunctional mitochondria to autophagosomes for degradation through the autophagy pathway. The current review explores the concept that an impairment in the mitophagy system leads to the accelerated progression of renal pathology. A better understanding of the cellular and molecular events that govern mitophagy and dynamics in <jats:styled-content style="fixed-case">DN</jats:styled-content> may lead to improved therapeutic strategies.</jats:p></jats:sec><jats:sec><jats:title>Linked Articles</jats:title><jats:p>This article is part of a themed issue on Mitochondrial Pharmacology: Energy, Injury & Beyond. To view the other articles in this issue visit <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="http://dx.doi.org/10.1111/bph.2014.171.issue-8">http://dx.doi.org/10.1111/bph.2014.171.issue‐8</jats:ext-link></jats:p></jats:sec> Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? British Journal of Pharmacology |
| spellingShingle | Higgins, G C, Coughlan, M T, British Journal of Pharmacology, Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy?, Pharmacology |
| title | Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? |
| title_full | Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? |
| title_fullStr | Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? |
| title_full_unstemmed | Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? |
| title_short | Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? |
| title_sort | mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? |
| title_unstemmed | Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy? |
| topic | Pharmacology |
| url | http://dx.doi.org/10.1111/bph.12503 |