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Intraperitoneal ZP123 improves aged oocyte quality by restoring granulosa cell gap junctions and improving

Hui Teng¹, Qijun Xie², Cheng Zhou³

¹Department of Reproductive Medicine, Jinling Clinical Medical College, Nanjing Medical University, Nanjing, Jiangsu, 210002, China.

Journal of Ovarian Research

|May 23, 2026

Summary

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Oogenesis

Oogenesis

In human women, oogenesis produces one mature egg cell or ovum for every precursor cell that enters meiosis. This process differs in two unique ways from the equivalent procedure of spermatogenesis in males. First, meiotic divisions during oogenesis are asymmetric, meaning that a large oocyte (containing most of the cytoplasm) and minor polar body are produced as a result of meiosis I, and again following meiosis II. Since only oocytes will go on to form embryos if fertilized, this unequal...

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This summary is machine-generated.

Female reproductive aging impairs fertility due to decreased oocyte quality linked to connexin 43 (CX43) gap junctions. The peptide ZP123 restored ovarian function and oocyte competence in aged mice, offering a potential therapy for age-related fertility decline.

Area of Science:

Reproductive Biology
Cellular Biology
Gerontology

Background:

Female fertility declines with age due to oocyte quality deterioration.
Oocyte maturation relies on granulosa cell communication via connexin 43 (CX43) gap junctions.
Age-related decline in CX43-mediated communication's impact on oocyte quality is not fully understood.

Purpose of the Study:

To investigate age-related changes in CX43 gap junction communication in the ovary.
To determine if the peptide ZP123 can restore CX43-mediated coupling and improve fertility in aged females.

Main Methods:

Assessed CX43 expression and phosphorylation in aged mouse ovaries and granulosa cells.
Evaluated ZP123 effects on gap junction communication in vitro (KGN cells) and in vivo (aged mice).

Keywords:

Aging CX43 Gap junction Granulosa cells Oocyte ZP123

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Analyzed oocyte maturation, spindle/mitochondrial function, ATP production, ROS levels, and embryo development in ZP123-treated aged mice.

Main Results:

CX43 expression and phosphorylation decreased with age in mouse ovaries.
ZP123 enhanced gap junction communication, improved follicle development, and oocyte maturation rates in aged mice.
ZP123 treatment restored mitochondrial function, reduced oxidative stress, and increased blastocyst formation rates.

Conclusions:

Disrupted CX43-mediated communication is a key factor in age-related oocyte quality decline.
Enhancing gap junction function with ZP123 effectively restored ovarian function and oocyte developmental potential.
Gap junction modulation presents a novel therapeutic strategy for mitigating age-related fertility loss.