ReviewAntioxidants (Basel, Switzerland)2026
HPV Infection and Oxidative Stress in Cervical Carcinogenesis: Linking Apoptosis, Senescence, SASP, and EMT.
Review in Antioxidants (Basel, Switzerland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cervical cancer (CC) is a complex, multistep process involving various viral, molecular, cellular, endogenous, and environmental events that transform normal cervical epithelium into a malignant tumor through a cascade of events. The contribution of high-risk human papillomavirus (HPV) to cancer is significant but involves many additional mechanisms such as oxidative stress (OS), arrested apoptosis of non-functional intraepithelial neoplastic cells, senescence-associated secretory phenotype (SASP), and the final epithelial-mesenchymal transition (EMT) of cervical epithelial neoplasia (CIN) cells. While high-risk HPV oncoproteins E6 and E7 are widely recognized as the primary triggers of CC, the critical role of E6 in degrading the p53 regulatory protein, thereby inhibiting the apoptosis of reactive oxygen species (ROS)-damaged neoplastic cells, is frequently underappreciated in the gynecological literature. Arrested apoptosis of non-functional neoplastic intraepithelial cells is a key event in cervical carcinogenesis and the biological basis of CIN progression via SASP senescence and ultimately EMT. While recent reviews touched upon each of the reviewed aspects, this review aims to provide a general understanding of all links in this complex molecular-biological chain, from HPV infection, oxidative stress, arrested apoptosis, SASP, and EMT. Beyond providing an encompassing primer for clinical researchers, we additionally review potential oxidative stress-related markers for shifting the classic diagnostic and therapeutic paradigms of CIN and cervical cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.