International Clinical and Medical Case Reports Journal (ISSN: 2832-5788) | Volume 4, Issue 11 | Research Article | Open Access
Wenli Chen*
Department of General Surgery, The Afffliated Bozhou Hospital of Anhui Medical University, China
*Correspondence to: Wenli Chen
Fulltext PDFBackground: Appendicitis is an acute inflammatory disorder driven by PI3K/Akt pathway hyperactivation, and 3-phosphoinositide-dependent protein kinase 1 (PDK1)—the upstream activator of Akt—modulates pro-inflammatory signaling and epithelial cell damage.
Objective: To synthesize basic experimental evidence on PDK1’s role in appendicitis and explore nursing relevance.
Methods: Retrospective analysis of PubMed (2019–2024) using keywords “Appendicitis[MeSH] AND PDK1[MeSH] AND Basic Research[Filter]”. Eligible studies were animal/cell models focusing on PDK1 in appendicitis.
Results: Ten studies were included. PDK1 activation (phosphorylation, p-PDK1) was upregulated in appendiceal tissues of animal models (mouse/rat) and LPS-stimulated cells, correlating with activated Akt, elevated pro-inflammatory cytokines (TNF-α, IL-6), and epithelial apoptosis. PDK1 inhibition alleviated inflammation and barrier damage.
Conclusion: PDK1 promotes inflammatory progression in appendicitis, providing a basis for nursing strategies in inflammation control and infection prevention.
Appendicitis; Inflammatory signaling; Hyperactivation; Barrier damage
Chen W. Phosphoinositide-Dependent Protein Kinase 1 (PDK1) in Appendicitis. Int Clinc Med Case Rep Jour. 2025;4(11):1-5.