Menopause related hormonal and inflammatory regulation of BCL2-mediated apoptosis in cervical cancer: A Systematic review

Authors

  • Amanda Fransisca Rhevytasari Department of Midwifery, Faculty of Medicine, Universitas Brawijaya, Malang, East Java, Indonesia
  • Arini Widya Risanti Department of Midwifery, Faculty of Medicine, Universitas Brawijaya, Malang, East Java, Indonesia
  • Tatit Nurseta Department of Midwifery, Faculty of Medicine, Universitas Brawijaya, Malang, East Java, Indonesia
  • Safrina Dewi Ratnaningrum Department of Midwifery, Faculty of Medicine, Universitas Brawijaya, Malang, East Java, Indonesia
  • Sutrisno Sutrisno Department of Obstetrics and Gynaecology, Faculty of Medicine, Universitas Brawijaya, Saiful Anwar General Hospital, Malang East Java, Indonesia
  • Agustina Tri Endarti Department of Medicine, Doctoral Program in Medical Science, Faculty of Medicine, Universitas Brawijaya, Malang, East Java, Indonesia

DOI:

https://doi.org/10.35816/jiksh.v15i2.303

Keywords:

apoptosis, BCL2 protein, cervical cancer, Inflammation, menopause

Abstract

Introduction: Menopause is characterized by a decline in estrogen levels that may alter inflammatory signaling and apoptotic regulation. Dysregulation of apoptosis, particularly involving B-cell lymphoma-2 (Bcl2), plays a critical role in cervical cancer progression. This systematic review aimed to synthesize current evidence on menopause-related hormonal changes and inflammatory mechanisms in regulating Bcl2-mediated apoptosis in cervical cancer.

Research Methodology: This systematic review followed PRISMA 2020 guidelines. Literature searches were conducted in October 2025 using PubMed and ScienceDirect. Eligible studies included human and animal research examining menopause-related hormonal status, inflammation, and Bcl2-associated apoptotic pathways in cervical cancer. Risk of bias was assessed using the Cochrane RoB 2 tool for human studies and the SYRCLE tool for animal studies. Due to heterogeneity, data were synthesized narratively.

Results: Six studies (2 human, 4 animal) published between 2019 and 2024 were included. Human studies demonstrated menopause-associated inflammatory changes, including elevated cytokines (IL-1α, IL-6, CRP), suggesting a pro-inflammatory environment relevant to apoptosis regulation. Animal studies consistently showed downregulation of Bcl2 and upregulation of pro-apoptotic markers (BAX, caspase-3), indicating mitochondrial apoptosis activation under estrogen-deprived conditions. Quantitative effect measures (e.g., OR, RR) were not consistently reported due to the predominance of mechanistic and preclinical designs.

Conclusion: Menopause-related hormonal decline is associated with increased inflammation and modulation of Bcl2-dependent apoptotic pathways in cervical cancer. While preclinical evidence strongly supports a mechanistic link, clinical evidence remains limited. Future translational studies integrating molecular, hormonal, and inflammatory biomarkers are needed to establish clinical relevance.

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References

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Published

13-07-2026

How to Cite

Fransisca Rhevytasari, A., Widya Risanti, A., Nurseta, T., Dewi Ratnaningrum, S., Sutrisno, S., & Tri Endarti, A. (2026). Menopause related hormonal and inflammatory regulation of BCL2-mediated apoptosis in cervical cancer: A Systematic review. Jurnal Ilmiah Kesehatan Sandi Husada, 15(2), 372–384. https://doi.org/10.35816/jiksh.v15i2.303

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