Publications by authors named "A J Kuret"
Vascular smooth muscle cells (VSMCs) can switch from their contractile state to a synthetic phenotype resulting in high migratory and proliferative capacity and driving atherosclerotic lesion formation. The cysteine-rich LIM-only protein 4 (CRP4) reportedly modulates VSM-like transcriptional signatures, which are perturbed in VSMCs undergoing phenotypic switching. Thus, we hypothesized that CRP4 contributes to adverse VSMC behaviours and thereby to atherogenesis in vivo.
View Article and Find Full Text PDF3',5'-cyclic guanosine monophosphate (cGMP) is a druggable second messenger regulating cell growth and survival in a plethora of cells and disease states, many of which are associated with hypoxia. For example, in myocardial infarction and heart failure (HF), clinical use of cGMP-elevating drugs improves disease outcomes. Although they protect mice from ischemia/reperfusion (I/R) injury, the exact mechanism how cardiac cGMP signaling is regulated in response to hypoxia is still largely unknown.
View Article and Find Full Text PDFArticle Synopsis
- - The 3',5'-cGMP pathway enhances the survival of heart cells during ischaemia and reperfusion injury by triggering protective responses, primarily through nitric oxide (NO)-sensitive guanylate cyclase (GC) which leads to cGMP production.
- - The activation of cGMP-dependent protein kinase I (cGKI) by cGMP results in the phosphorylation of various substrates, promoting the opening of mitochondrial ATP-sensitive potassium channels (mitoK) and BK-type calcium-activated potassium channels (mitoBK).
- - Agents that activate mitoK or mitoBK can help protect against damage caused by ischemia and reperfusion, suggesting that the relationship between the cGMP pathway and these
Article Synopsis
- The Slack potassium channel (also known as Slo2.2 or Kcnt1) plays a crucial role in stabilizing the resting membrane potential and regulating neuronal excitability, particularly under high sodium conditions.
- Research using Slack-deficient and wild-type mice revealed that the absence of Slack increases susceptibility to excitotoxic damage from overstimulation of glutamate receptors, leading to greater brain lesions in Slack KO mice.
- Additionally, the study indicated that Slack channels help protect neurons from cell death in excitotoxic environments through mechanisms involving neurotrophin receptor activation and the regulation of potassium levels during receptor stimulation.