As ovaries age, supporting tissue grows stiffer, and slowing this change may help extend fertility. The area between cells forms a gel-like substance filled with proteins and molecules that support suspended cells. It also transmits chemical and mechanical signals between cells, known as the extracellular matrix. Firmness of this matrix differs throughout the ovary. Primordial follicles hold immature eggs awaiting development. These structures lack blood supply and connect to other cells only through the matrix. To protect them, the matrix stays stiff and regulated. Around maturing follicles, the matrix softens to allow nutrient delivery and growth space. Factors such as oxidative stress and chronic inflammation influence ovarian aging. After decades, ovaries display fibrosis and matrix stiffening from collagen buildup. This stiffening impairs egg development and may influence menopause timing. Researchers from Huazhong University of Science and Technology showed a method to keep the ovarian matrix more flexible in mice. The approach could support treatments that delay menopause and lengthen reproductive years. It targets the signaling protein interleukin 11 (IL-11). Ovarian matrix stiffening depends critically on IL-11, the authors note. Blocking the IL-11 pathway reduces stiffness, improves ovarian function in aging, and counters various disease factors. They first studied signs of ovarian aging in humans using samples from different age groups and patients with ovarian issues. Findings linked aging and certain conditions to increased matrix stiffness. RNA sequencing and proteomics identified IL-11 as a driver of fibroblast activation. IL-11 levels rose with age across mice, rats, and humans. Inhibiting IL-11 signaling in mice lowered stiffness and collagen while increasing pups per litter. Human treatments remain distant, though anti-IL-11 trials for other conditions are underway.
