Al-Kunooze Scientific Journal

Hypoxia promotes cellular apoptosis in blood cells through P53 activation in patients with Diabetes

Document Type : Original Article

Authors

Azhar Abul Jabbar Ameen 1
zyad abdulkadhim mazyed 2
Suhyila Fadhil Ali 2

1 Basrah university \\\\College of Science

2 Biology\college of science\Basrah university\Basrah\Iraq

https://doi.org/10.36582/ksj.2026.170052.1034
Abstract
Hyperglycemia in diabetes promotes Hypoxia leading to alterations in the cellular microenvironment, Hypoxia triggers adaptive cellular responses, that are largely regulated via a transcription factor called Hypoxia inducible factor 1 -alpha (HIF-1α),in addition Hypoxia influences cell death pathways through the stabilization of the tumor suppressor factor p53.Aims: this study aims to assess the impact of hypoxia inducible factor (HIF-1α) in regulating p53 signaling in those with type 2 diabetes in comparison with the control group. Whole blood samples were obtained from both diabetes and non-diabetic participants, followed by quantitative PCR (qPCR) to estimate the relative transcriptional levels of (HIF-1α and p53). The results showed a significant up regulation in the expression of HIF-1α and p53inpatientsrelative to the control group, Analysis of covariance (ANCOVA) revealed that the overall model for HIF-1α and P53 expression was statistically significant, while diabetes status, gender and body mass index (BMI) did not show significant in dependent effects. Additionally a notable positive correlation was observed between expression of HIF-1α and p53. The study illustrated that a potential impact of theHIF-1α signaling in inducing cellular apoptosis through the upregulating of p53, these results provide evidencethatHIF-1α and p53 may act as interconnected cellular markers and support further investigation in expanded cohorts.

Keywords

Cellular apoptosis
Hyperglycemia
Blood microenvironment
Diabetes mellitus
Hypoxia inducible factor
Subjects
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Al-Kunooze Scientific Journal
Volume 12, Issue 3
Summer 2026
Pages 31-45

  • Receive Date 14 March 2026
  • Revise Date 17 April 2026
  • Accept Date 17 April 2026
  • First Publish Date 25 June 2026
  • Publish Date 01 July 2026

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