ArticleJournal of cellular and molecular medicine2022
Kallistatin prevents ovarian hyperstimulation syndrome by regulating vascular leakage.
Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Unveiling the role of the PI3K/Akt signaling pathway in follicular development and non-malignant ovarian dysfunction: a comprehensive review.Journal of ovarian research · 2026Review
- Effect of Nifedipine in Preventing Ovarian Hyperstimulation Syndrome through TRPC1 Ion Channel Inhibition.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Minimising OHSS in women with PCOS.Frontiers in endocrinology · 2025Review
- Kallistatin as a Potential Biomarker in Polycystic Ovary Syndrome: A Prospective Cohort Study.Diagnostics (Basel, Switzerland) · 2024Article
- Vitamin DIn vitro cellular & developmental biology. Animal · 2024Article
- Kallistatin prevents ovarian hyperstimulation syndrome by regulating vascular leakage.Journal of cellular and molecular medicine · 2022Article
- EGR1 Promotes Ovarian Hyperstimulation Syndrome Through Upregulation of SOX9 Expression.Cell transplantationArticle
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Angiogenesis and increased permeability are essential pathological basis for the development of ovarian hyperstimulation syndrome (OHSS). Kallistatin (KS) is an endogenous anti-inflammatory and anti-angiogenic factor that participates in a variety of diseases, but its role in OHSS remains unknown. In this study, treating a human ovarian granulosa-like tumour cell line KGN and human primary granulosa cells (PGCs) with human chorionic gonadotropin (hCG) reduced the expression of KS, but increased the expression of VEGF. Furthermore, we found that KS could attenuate the protein level of VEGF in both KGN cells and human PGCs. More interestingly, we observed that exogenous supplementation of KS significantly inhibited a series of signs of OHSS in mice, including weight gain, ovarian enlargement, increased vascular permeability and up-regulation of VEGF expression. In addition, KS was proved to be safe on mice ovulation, progression of normal pregnancy and fetus development. Collectively, these findings demonstrated that KS treatment prevented OHSS, at least partially, through down-regulating VEGF expression. For the first time, these results highlight the potential preventive value of KS in OHSS.
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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.