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Melatonin antagonizes ovarian aging via YTHDF2-MAPK-NF-κB pathway
Ruigong Zhu1, Xian Ji1, Xuan Wu1
1Key Laboratory of Cardiovascular & Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing, Jiangsu 211166, PR China.
Genes & Diseases
|February 28, 2022
Summary
Melatonin protects human ovarian surface epithelial cells from aging by inhibiting the ROS-YTHDF2-MAPK-NF-κB pathway. This discovery offers new strategies for delaying ovarian aging and related reproductive diseases.
Area of Science:
- Reproductive biology
- Cellular senescence
- Epigenetics
Background:
- Cellular senescence is linked to age-related diseases, with ovarian aging being a key factor in reproductive system disorders.
- Ovarian aging involves loss of epithelial integrity and reduced human ovarian surface epithelial cell (HOSEpiC) numbers.
Purpose of the Study:
- To investigate the epigenetic mechanisms of melatonin in protecting HOSEpiCs against aging.
- To explore melatonin's role in delaying ovarian aging.
Main Methods:
- Investigated the effects of melatonin on oncogene-induced senescence (OIS) in HOSEpiCs.
- Examined the role of YTHDF2, a reader of RNA N6-methyladenosine (m6A), in the senescence pathway.
- Analyzed the involvement of ROS, MAP2K4, MAP4K4, and NF-κB signaling in OIS.
Main Results:
- Melatonin demonstrated antagonistic effects against OIS in HOSEpiCs.
- The oncogene Ras reduced YTHDF2 expression via reactive oxygen species (ROS) generation.
- Suppression of YTHDF2 stabilized mRNA transcripts of MAP2K4 and MAP4K4, activating the MAP2K4/MAP4K4-dependent NF-κB pathway and upregulating senescence-associated secretory phenotype (SASP).
Conclusions:
- Melatonin counteracts OIS in HOSEpiCs by inhibiting the ROS-YTHDF2-MAPK-NF-κB pathway.
- Findings offer insights into potential therapeutic strategies for preventing and treating ovarian aging.
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