AI Article Synopsis
- Lipopolysaccharide (LPS), found in the outer membrane of Gram-negative bacteria, triggers inflammation by activating toll-like receptors (TLRs) through pathways like MyD88 and TRIF.
- Research indicates that LPS-related inflammatory responses can lead to ovarian dysfunction and reduced female fertility, though the reasons are complicated.
- This review explores various studies on LPS and fertility decline, aiming to clarify how LPS affects female reproductive health and proposes potential therapeutic strategies to mitigate its impact.
Article Abstract
As a major component of the outer membrane of Gram-negative bacteria, lipopolysaccharide (LPS) can be recognized by toll-like receptors (TLRs) and induce inflammation through MyD88 or the TIR domain-containing adapter-inducing interferon-β (TRIF) pathway. Previous studies have found that LPS-associated inflammatory/immune challenges were associated with ovarian dysfunction and reduced female fertility. However, the etiology and pathogenesis of female fertility decline associated with LPS are currently complex and multifaceted. In this review, PubMed was used to search for references on LPS and fertility decline so as to elucidate the potential mechanisms of LPS-associated female fertility decline and summarize therapeutic strategies that may improve LPS-associated fertility decline.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11534943 | PMC |
| http://dx.doi.org/10.1007/s10815-024-03226-2 | DOI Listing |
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