ArticleFrontiers in psychiatry2019
An Analysis of Cellular Communication Network Factor Proteins as Candidate Mediators of Postpartum Psychosis Risk.
Article in Frontiers in psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Does hypothalamic CCN3 hypersecretion confer postpartum mood disorder risk?Translational psychiatry · 2026Review
- Differentially expressed transcripts associated with depressive symptoms during pregnancy and postpartum.Molecular psychiatry · 2025Article
- Genetic and Epigenetic Factors Associated with Postpartum Psychosis: A 5-Year Systematic Review.Journal of clinical medicine · 2024Review
- Cellular communication network factor 3 in cartilage development and maintenance.Journal of cell communication and signaling · 2021Review
- A new molecular risk pathway for postpartum mood disorders: clues from steroid sulfatase-deficient individuals.Archives of women's mental health · 2021Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Postpartum (or puerperal) psychosis (PP) is a severe psychiatric condition associated with hallucinations, delusions, cognitive disorganization, and mood problems, which affects approximately 1-2 out of every 1,000 mothers shortly after childbirth. While the risk factors for, and co-morbidities of, PP are relatively well-defined, currently, the pathophysiology underlying the disorder is very poorly-specified. Here, I argue, on the basis of multiple lines of new evidence, that altered expression of the Cellular Communication Network (CCN) factor proteins (and of the heterodimerizing CCN2 and CCN3 proteins in particular), may be associated with, and possibly causal for, increased PP risk. Future preclinical and clinical studies should aim to test this hypothesis as empirical support for it would provide much-needed clues regarding the biological substrates of PP, and could point to predictive biomarkers for the condition.
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Registered trials
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