ReviewBiomedical reports2022
Potential role of β-carotene-modulated autophagy in puerperal breast inflammation (Review).
Review in Biomedical reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed, 3 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Puerperal breast inflammation is common in the first 6-8 weeks postpartum, and without proper management, may lead to a decrease in breastmilk production and early cessation of breastfeeding. Recent studies showed that carotenoids decrease the severity of puerperal breast inflammation. This article summarizes the significant findings on β-carotene with a potential role as an autophagy modulator in puerperal breast inflammation. Puerperal milk stasis causes an increase in inflammatory cytokines and inflammatory cells, leading to reactive oxygen species (ROS) activation that causes oxidative damage to mammary glands and affects breast milk secretion. β-carotene has an anti-inflammatory effect related to its ROS-scavenging activity and modulates autophagy, thus stimulating the removal of damaged cellular structures and supporting milk gland survival. β-carotene modulates autophagy through phosphorylation of NF-κB, JNK, p38, Akt, and Nrf2, affects the ratio of Microtubule-associated protein 1A/1B-light chain 3 (LC3)-II/LC3-I, and has a role in the regulation of the JAK2/STAT3, PI2K/Akt/mTOR and AMPK pathways. Although the
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Registered trials
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