Abstract：
:Acute kidney injury (AKI) is defined as a rapid loss of kidney function characterised by inflammation and cell death, ultimately leading to further functional and structural renal alterations. Based on experimental and epidemiological pieces of evidence, AKI may progress to chronic kidney disease (CKD) even after a recovery period due to maladaptive repair and other underlying mechanisms such as heightened Wnt signalling, overstimulation of the renin-angiotensin-aldosterone-system (RAAS) pathway, epigenetic alterations and inhibition of hypoxia-inducible factor (HIF) dependent defences. It has been reported that RAAS activation subsequent to renal insult mediates inflammatory and fibrotic mechanisms, which are a hallmark of CKD. Moreover, interesting evidence regarding the exposure-dependent dual role of Wnt signalling in both injury and repair, epigenetic changes underlying kidney disease suggest a potential therapeutic role of these pathways in AKI to CKD continuum. In addition, the hypoxia-independent renal benefits of erythropoietin such as anti-apoptosis and tubular regeneration also present an auspicious target which could be useful in clinical settings. In this review, the specific roles of these pathways in kidney disease, their pathological mechanisms and therapeutic strategies are discussed. Moreover, notable reports concerning stem cell therapy which hold promise in halting AKI-CKD continuum will be elaborated.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Ogbadu J,Singh G,Aggarwal Ddoi
10.1016/j.ejphar.2019.172711subject
Has Abstractpub_date
2019-12-15 00:00:00pages
172711eissn
0014-2999issn
1879-0712pii
S0014-2999(19)30663-6journal_volume
865pub_type
杂志文章,评审abstract：:Overproduction of the free radical nitric oxide (NO) has been implicated in the pathogenesis of a variety of inflammatory and immunologically mediated diseases as well as complications of diabetes. In the present study we have demonstrated that aminoguanidine selectively inhibits the cytokine-inducible isoform of NO s...
journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/0014-2999(93)90357-n
更新日期：1993-03-16 00:00:00
abstract：:In adult male rats, injection of TRH into a lateral ventricle of the brain 5 min prior to pentobarbital (PB) administration caused a significant dose-related inhibition of prolactin (PRL) release, in doses ranging from 500 to 5 ng. Among 8 TRH analogues devoid of thyrotropin-releasing activity, 6 were found to signifi...
journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/0014-2999(77)90276-x
更新日期：1977-10-15 00:00:00
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/j.ejphar.2013.05.009
更新日期：2013-09-05 00:00:00
abstract：:Propofol is generally used for the induction and maintenance of anesthesia in clinical procedures via activation of γ -aminobutyric acid A (GABAA) receptors. When administered at the clinical dose, propofol use is associated with movement disorders, including dystonia and ataxia, suggesting that propofol administratio...
journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/j.ejphar.2020.173474
更新日期：2020-11-15 00:00:00
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/0014-2999(93)90704-l
更新日期：1993-03-30 00:00:00
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/0014-2999(90)90362-a
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/0922-4106(95)90142-6
更新日期：1995-10-15 00:00:00
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/0014-2999(84)90353-4
更新日期：1984-06-15 00:00:00
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/j.ejphar.2019.01.041
更新日期：2019-04-05 00:00:00
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/0014-2999(90)90180-e
更新日期：1990-04-25 00:00:00
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journal_title：European journal of pharmacology
pub_type： 杂志文章,评审
doi：10.1016/j.ejphar.2005.12.057
更新日期：2006-03-08 00:00:00
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/j.ejphar.2003.12.036
更新日期：2004-02-23 00:00:00
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/j.ejphar.2020.173671
更新日期：2021-01-15 00:00:00
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/0014-2999(94)90201-1
更新日期：1994-03-03 00:00:00
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/s0014-2999(99)00666-4
更新日期：1999-11-19 00:00:00
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/s0014-2999(98)00341-0
更新日期：1998-07-03 00:00:00
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/j.ejphar.2006.12.037
更新日期：2007-04-30 00:00:00
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/j.ejphar.2007.04.012
更新日期：2007-07-30 00:00:00
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/0014-2999(77)90063-2
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/0014-2999(78)90324-2
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/0014-2999(88)90257-9
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/s0014-2999(02)02248-3
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journal_title：European journal of pharmacology
pub_type： 杂志文章,评审
doi：10.1016/j.ejphar.2010.02.003
更新日期：2010-05-10 00:00:00
abstract：:2-Arachidonylglycerol (2-AG) inhibits the production in vitro of tumor necrosis factor-alpha (TNF-alpha) by mouse macrophages, as well as in mice. It has no effect on the production of nitric oxide (NO). The effect on TNF-alpha is enhanced when 2-AG is administered together with 2-linoleylglycerol (2-Lino-G) and 2-pal...
journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/s0014-2999(00)00653-1
更新日期：2000-10-06 00:00:00
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journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/j.ejphar.2008.03.047
更新日期：2008-06-10 00:00:00
abstract：:The significance of the blood pressure elevation caused by N(G)-nitro-L-arginine (L-NNA) to inhibitory mechanism of the drug on depressor responses to acetylcholine in anesthetized dogs was investigated. L-NNA (50 mg kg(-1), i.v.) elevated blood pressure to a plateau of 30-50 mm Hg above baseline level and shifted the...
journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/s0014-2999(99)00288-5
更新日期：1999-06-04 00:00:00
abstract：:Activating mutations in FMS-like tyrosine kinase 3 (FLT3) occur in 25% of acute lymphoid and 30% of acute myeloid leukaemia cases. Therefore, FLT3 is a potential therapeutic target for small molecule kinase inhibitors. In this study, protein-ligand interactions between FLT3 and kinase inhibitors (CEP701, PKC412, sunit...
journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/j.ejphar.2016.02.048
更新日期：2016-04-05 00:00:00
abstract：:The beta-carboline FG7142 is a partial inverse agonist at benzodiazepine receptors. We have shown previously that a single dose of this drug causes an upregulation of cortical beta-adrenoceptor numbers in mouse cerebral cortex. This rise was seen seven days, but not 15-30 min or 24 h after FG7142 administration. We no...
journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/0014-2999(87)90255-x
更新日期：1987-07-09 00:00:00
abstract：:The effects of morphine (0.1 mg/kg) and 5-HTP (2 mg/kg) on colonic motility were investigated in dogs fasted for 15-22 h and fitted with two strain gauge transducers on the transverse colon at 8 and 12 cm from the ileo-colonic junction. The effects were compared to those obtained after previous intravenous (i.v.) (0.2...
journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/0014-2999(82)90503-9
更新日期：1982-08-27 00:00:00
abstract：:Inhibition of intrathecal substance P-elicited behavior by mu-, delta- and kappa-opioids was compared. In both the substance P behavioral test and the tail flick antinociceptive test, intrathecal [D-Ala2, Met5]enkephalinamide and [D-Ala2, D-Leu5]enkephalin (DADL) were equipotent, morphine and ethylketazocine were less...
journal_title：European journal of pharmacology
pub_type： 杂志文章
doi：10.1016/0014-2999(82)90403-4
更新日期：1982-12-17 00:00:00
