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Promoting Mitochondrial Biogenesis w...

Funk, Jason Allen.

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Promoting Mitochondrial Biogenesis with the SIRT1 Activator SRT1720 to Improve Mitochondrial and Renal Function after Acute Kidney Injury.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Promoting Mitochondrial Biogenesis with the SIRT1 Activator SRT1720 to Improve Mitochondrial and Renal Function after Acute Kidney Injury./
作者:	Funk, Jason Allen.
面頁冊數:	200 p.
附註:	Source: Dissertation Abstracts International, Volume: 74-04(E), Section: B.
Contained By:	Dissertation Abstracts International74-04B(E).
標題:	Health Sciences, Pharmacology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3533532
ISBN:	9781267777287

Promoting Mitochondrial Biogenesis with the SIRT1 Activator SRT1720 to Improve Mitochondrial and Renal Function after Acute Kidney Injury.
Funk, Jason Allen.

Promoting Mitochondrial Biogenesis with the SIRT1 Activator SRT1720 to Improve Mitochondrial and Renal Function after Acute Kidney Injury. - 200 p.

Source: Dissertation Abstracts International, Volume: 74-04(E), Section: B.

Thesis (Ph.D.)--Medical University of South Carolina, 2012.

Mitochondrial dysfunction is a primary pathological consequence of acute kidney injury (AKI). Induction of mitochondrial biogenesis via the nuclear coactivator of transcription PPARgamma-coactivator-1alpha (PGC-1alpha), the master regulator of mitochondrial biogenesis, rescues mitochondrial function in renal cells after oxidant injury. The primary goal of this project was to evaluate the recovery of mitochondrial function after in vivo AKI, and to determine the influence of mitochondrial biogenesis during the repair process.

ISBN: 9781267777287Subjects--Topical Terms:

1017717
Health Sciences, Pharmacology.

Promoting Mitochondrial Biogenesis with the SIRT1 Activator SRT1720 to Improve Mitochondrial and Renal Function after Acute Kidney Injury.
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245 1 0 $a Promoting Mitochondrial Biogenesis with the SIRT1 Activator SRT1720 to Improve Mitochondrial and Renal Function after Acute Kidney Injury.
300 $a 200 p.
500 $a Source: Dissertation Abstracts International, Volume: 74-04(E), Section: B.
500 $a Adviser: Rick G. Schnellmann.
502 $a Thesis (Ph.D.)--Medical University of South Carolina, 2012.
520 $a Mitochondrial dysfunction is a primary pathological consequence of acute kidney injury (AKI). Induction of mitochondrial biogenesis via the nuclear coactivator of transcription PPARgamma-coactivator-1alpha (PGC-1alpha), the master regulator of mitochondrial biogenesis, rescues mitochondrial function in renal cells after oxidant injury. The primary goal of this project was to evaluate the recovery of mitochondrial function after in vivo AKI, and to determine the influence of mitochondrial biogenesis during the repair process.
520 $a Deacetylation of PGC-1alpha by the class III HDAC SIRTI produces a more active form of the protein and stimulates mitochondrial biogenesis. The potent SIRT I activator SRT1720 induced deacetylation of PGC-1alpha, increased mitochondrial proteins, and elevated mitochondrial respiration and total cellular ATP levels in primary renal proximal tubule cell (RPTC) cultures. The effects of SRT1720 occurred in a SIRTI-dependent manner and exposure of SRT1720 following oxidant injury to RPTC expedited recovery of mitochondrial and cellular functions.
520 $a Acute kidney injury (AKI), either by ischemia-reperfusion (UR) or glycerol-induced myoglobinuric injury, produced persistent proximal tubule damage even in the face of recovered glomerular filtration. Tubule pathology was determined histologically, by the continued presence of dilated, flattened tubules, and the loss of Na +,K+-ATPase expression. The persistent tubule injury was associated with sustained loss of mitochondrial protein expression, alterations in fusion/fission proteins, and elevated mitochondrial biogenesis proteins.
520 $a Treating with SRT1720 after I/R injury in rats induced PGC-1alpha deacetylation and restored mitochondrial protein expression and function by 144h after reperfusion, but not at 72h. Restoration of mitochondrial function was associated with attenuated kidney injury molecule-1 (Kim-1), recovery of Na+,K +-ATPase expression and localization, and normalized vimentin expression. The results suggested that recovery of mitochondrial function correlates with faster recovery of a normal, differentiated, polarized proximal tubule epithelium.
520 $a Taken together, we have demonstrated that mitochondrial biogenesis is an essential component of renal cell repair following AKI, and by promoting faster recovery of mitochondrial function, we can expedite recovery of the differentiated tubule epithelium with basolateral-apical polarity. These discoveries may ultimately point towards new therapeutic techniques that can be further examined as potential interventions to treat AKI and other disorders associated with sustained mitochondrial dysfunction.
590 $a School code: 0122.
650 4 $a Health Sciences, Pharmacology. $3 1017717
650 4 $a Health Sciences, Toxicology. $3 1017752
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710 2 $a Medical University of South Carolina. $3 700119
773 0 $t Dissertation Abstracts International $g 74-04B(E).
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791 $a Ph.D.
792 $a 2012
793 $a English
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