Current Perspective : Regeneration of Injured Renal Tubules
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- Yoshida Makoto
- Department of Pharmacology, Faculty of Pharmacy, Takasaki University of Health and Welfare, Japan
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- Honma Shigeyoshi
- Department of Pharmacology, Faculty of Pharmacy, Takasaki University of Health and Welfare, Japan
書誌事項
- タイトル別名
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- Regeneration of Injured Renal Tubules
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抄録
Acute kidney injury (AKI), clinically defined by high serum creatinine and low urine flow, has many complicated pathophysiological features including tubular and glomerular injury. Although renal tubules are thought to be constituted by highly differentiated epithelial cells, it is possible to repair injured nephrons by the healing process. Several studies have revealed that AKI, especially AKI caused by ischemia/reperfusion injury or nephrotoxic medication, depends on a number of factors, including activation of transcriptional factors, endothelial injury of peritubular small vessels, immune responses, and inflammatory processes associated with necrosis and apoptosis of renal tubular epithelium. For regeneration of injured tubules, partly dedifferentiated progenitor-like cells fill the injured site and constitute the tubular structure and function, although the source of these cells is still under debate. It is essential to understand the molecular, cellular, and genetic mechanisms of AKI and tubular regeneration for the development of therapies to prevent and treat kidney injury.
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 124 (2), 117-122, 2014
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001205179572224
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- NII論文ID
- 130003391487
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- NII書誌ID
- AA11806667
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- COI
- 1:CAS:528:DC%2BC2cXkt1egtro%3D
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 025296068
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- PubMed
- 24463777
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可