ReviewMolecular biology reports2025
TAp73 as a potential key for understanding male infertility: a mini-review.
Review in Molecular biology reports, 2025. 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.
- Wuzi-Yanzong-Wan inhibits testicular mitochondrial apoptosis in rats by downregulating TAp73-Mediated P38 MAPK-ADAM17 pathway.Frontiers in pharmacology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infertility is a significant global reproductive health issue, impacting 9% of couples, with male factors contributing to approximately 50% of cases. Infertility in men can be caused by genetics, lifestyle, obesity, or several diseases, like oligozoospermia. In oligozoospermia, one of the most common diseases in male infertility, sperm concentration is less than 15 million/ml, and is graded as moderate, mild, and severe according to the decreasing concentration. In males,, following the onset of puberty, a complex process occurs with the contribution of many genes and proteins, resulting in the production of spermatids through mitotic and meiotic divisions from spermatogonia, a process known as spermatogenesis. The well-known p53 family, including p53, p63, and p73 transcription factors, plays an important role during spermatogenesis. It has been shown that while sperm count increased in p53 and p63 knockout mice, abnormality in sperm morphology also increased. The isoform of p73 that contains only the transactivator domain is referred to as TAp73. A significant reduction in germ cell counts and sperm maturation due to deficiencies in the spermatogenesis process was observed in TAp73 knockout mice. Furthermore, a model for oligoasthenozoospermia, characterized by low sperm count and reduced motility, was developed by inhibiting TAp73. While the roles of p53 and p63 in spermatogenesis have been thoroughly explored, the precise function of TAp73 within this context remains unclear. This review aims to shed light on the potential importance of the TAp73 transcription factor in the development of oligozoospermia.
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Identifiers
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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 OpenQuestion graph.