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Molecular determinants of acute kidney injury.

Husi H, Human C - J Inj Violence Res (2015)

Bottom Line: However, no effective therapy for AKI exists.A major hurdle to devise a successful strategy is the multifactorial and complex nature of the disorder itself, whereby the activation of a number of seemingly independent molecular pathways in the kidney leads to apoptotic and necrotic events.Here we address the current understanding of the molecular pathways evoked in AKI, their interplay, and the potential to pharmacologically intervene in the effective prevention and/or progression of AKI.

View Article: PubMed Central - PubMed

Affiliation: BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, UK. Email: Holger.Husi@glasgow.ac.uk.

No MeSH data available.


Related in: MedlinePlus

Signaling cascades and evoked pathways involved in AKI. Known primary modulators of AKI (blue boxes) with downstream targets (yellow boxes) and hallmarks (green boxes) are shown. Grey boxes denote chemical compounds, and red boxes indicate endpoints in AKI.
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Figure 1: Signaling cascades and evoked pathways involved in AKI. Known primary modulators of AKI (blue boxes) with downstream targets (yellow boxes) and hallmarks (green boxes) are shown. Grey boxes denote chemical compounds, and red boxes indicate endpoints in AKI.

Mentions: A potential summary of AKI-modulated pathways and signaling events leading to Ca2+-overload and apoptosis as well as necrosis in kidney tissue after injury is shown in Figure 1.


Molecular determinants of acute kidney injury.

Husi H, Human C - J Inj Violence Res (2015)

Signaling cascades and evoked pathways involved in AKI. Known primary modulators of AKI (blue boxes) with downstream targets (yellow boxes) and hallmarks (green boxes) are shown. Grey boxes denote chemical compounds, and red boxes indicate endpoints in AKI.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4522318&req=5

Figure 1: Signaling cascades and evoked pathways involved in AKI. Known primary modulators of AKI (blue boxes) with downstream targets (yellow boxes) and hallmarks (green boxes) are shown. Grey boxes denote chemical compounds, and red boxes indicate endpoints in AKI.
Mentions: A potential summary of AKI-modulated pathways and signaling events leading to Ca2+-overload and apoptosis as well as necrosis in kidney tissue after injury is shown in Figure 1.

Bottom Line: However, no effective therapy for AKI exists.A major hurdle to devise a successful strategy is the multifactorial and complex nature of the disorder itself, whereby the activation of a number of seemingly independent molecular pathways in the kidney leads to apoptotic and necrotic events.Here we address the current understanding of the molecular pathways evoked in AKI, their interplay, and the potential to pharmacologically intervene in the effective prevention and/or progression of AKI.

View Article: PubMed Central - PubMed

Affiliation: BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, UK. Email: Holger.Husi@glasgow.ac.uk.

No MeSH data available.


Related in: MedlinePlus