ArticleMolecular endocrinology (Baltimore, Md.)2008
Female infertility and disrupted angiogenesis are actions of specific follistatin isoforms.
Article in Molecular endocrinology (Baltimore, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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
18 citing papers in PubMed, 46 citations in OpenAlex.
- PasteurizedNutrients · 2024Trial
- A common allele increases endometrial Wnt4 expression, with antagonistic implications for pregnancy, reproductive cancers, and endometriosis.Nature communications · 2024Article
- Technical opportunities and challenges in developing total-body PET scanners for mice and rats.EJNMMI physics · 2023Review
- Low follistatin level is a causal risk factor for spontaneous abortion: a two-sample mendelian randomization study.Frontiers in endocrinology · 2023Article
- HPhysics in medicine and biology · 2021Article
- Follistatin is critical for mouse uterine receptivity and decidualization.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Activins and Inhibins: Roles in Development, Physiology, and Disease.Cold Spring Harbor perspectives in biology · 2016Review
- Maternal protein restriction induces early-onset glucose intolerance and alters hepatic genes expression in the peroxisome proliferator-activated receptor pathway in offspring.Journal of diabetes investigation · 2015Article
- Inhibin at 90: from discovery to clinical application, a historical review.Endocrine reviews · 2014Review
- The effects of transforming growth factor-β2 on the expression of follistatin and activin A in normal and glaucomatous human trabecular meshwork cells and tissues.Investigative ophthalmology & visual science · 2012Article
- Cell-type specific modulation of pituitary cells by activin, inhibin and follistatin.Molecular and cellular endocrinology · 2012Review
- Follistatin improves skeletal muscle healing after injury and disease through an interaction with muscle regeneration, angiogenesis, and fibrosis.The American journal of pathology · 2011Article
- The Local Control of the Pituitary by Activin Signaling and Modulation.Open neuroendocrinology journal (Online) · 2011Article
- The follistatin-288 isoform alone is sufficient for survival but not for normal fertility in mice.Endocrinology · 2010Article
- Accelerated ovarian aging in the absence of the transcription regulator TAF4B in mice.Biology of reproduction · 2010Article
- The biology of activin: recent advances in structure, regulation and function.The Journal of endocrinology · 2009Review
- Keratinocyte-derived follistatin regulates epidermal homeostasis and wound repair.Laboratory investigation; a journal of technical methods and pathology · 2009Article
- Clinical and Therapeutic Implications of Follistatin in Solid Tumours.Cancer genomics & proteomicsReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
The circulating and tissue-bound forms of follistatin (FST315 and FST288, respectively) modulate the actions of activins. FST knockout (KO/null) mice, lacking both isoforms, die perinatally with defects in lung, skin, and the musculoskeletal system. Using constructs of the human FST gene engineered to enable expression of each isoform under the control of natural regulatory elements, transgenic mouse lines were created and crossed with FST null mice to attempt to rescue the neonatal lethality. FST288 expression alone did not rescue the neonatal lethality, but mice expressing FST315 on the KO background survived to adulthood with normal lung and skin morphology and partial reversal of the musculoskeletal defects noted in FST KO mice. The FST315 rescue mice displayed a short period of neonatal growth retardation, impaired tail growth, and female infertility. The latter may be due to failure of corpus luteum formation, a decline in the ovarian follicular population, and an augmented uterine inflammatory response to mating. Failure of corpus luteum formation and impaired tail growth indicate abnormal vascularization and suggest that FST288 is required for the promotion of angiogenesis. The augmented uterine inflammatory response may result from the failure of FST315 to modulate the proinflammatory actions of activin A in the uterus or may result from the altered steroid milieu associated with the ovarian abnormalities. Although we cannot definitively conclude that the remaining defects are due to the absence of a particular isoform or due to variable expression of each, these models have demonstrated novel physiological processes that are influenced by FST.
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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.