What this means
Researchers found that humanin helped human ovary cells and rat ovary tissue survive damage from oxidative stress. This was tested in cells and tissue, not people, so it does not show effects in humans.
Plain-English summary written by an AI model from the abstract. The original is below.
- Who it was tested in
- Human ovary cells in a lab dish and rat ovaries grown in culture
- Kind of research
- A study
The science
- Original title
- Mitochondrial-derived peptide Humanin protects granulosa cells under oxidative conditions.
- Authors
- Conte JG, Reynoso S, Gosso MS et al.
- Journal
- Reproduction (Cambridge, England)
- Published
- Jul 3, 2026
- Study type
- Study · in humans
- PMID
- 42397223 ↗
Abstract
In brief: Redox imbalance compromises granulosa cell survival and follicle fate. This study identifies the mitochondrial-derived peptide Humanin (HN) as a cytoprotective factor that protects granulosa cells under oxidative condItions. Abstract: Granulosa cell function is essential for proper ovarian physiology. Redox imbalance compromises granulosa cell survival, thereby impacting follicle fate within the ovary. Humanin (HN), a small mitochondrial-derived peptide, exerts cytoprotective effects in several tissues under pro-oxidant conditions. The present study aimed to evaluate the cytoprotective effects of HN under oxidative conditions in granulosa cells, using a human granulosa cell line (KGN) and an in-vitro rat ovary culture to assess its action within the ovarian microenvironment. KGN cells showed a significant increase in endogenous HN mRNA expression in response to oxidative conditions induced by H2O2. Upon oxidative insult, exogenous HN enhanced cellular antioxidant capacity by significantly increasing catalase activity levels, without modifying superoxide dismutase expression or activity, or redox status in KGN cells. Importantly, HN significantly decreased H2O2-induced granulosa cell apoptosis in KGN cells, as determined by the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. This protective effect was associated with modulation of key apoptosis-related genes, including reduced expression of BAX and the caspase-3 precursor (CASP3), while BCL2 expression remained unchanged. Consistently, in rat ovaries, HN protected granulosa cells of antral follicles under oxidative conditions. In conclusion, our findings support a cytoprotective role of HN in granulosa cells under oxidative conditions, which may contribute to the maintenance of antral follicle survival within the ovarian microenvironment.
Conte JG, Reynoso S, Gosso MS et al. Mitochondrial-derived peptide Humanin protects granulosa cells under oxidative conditions. Reproduction (Cambridge, England). 2026. doi:10.1093/reprod/xaag082. PMID: 42397223. https://pubmed.ncbi.nlm.nih.gov/42397223/
Related research
Humanin treatment eased heart damage in diabetic mice
Mice with diabetes that got daily humanin for 15 days had less stress, inflammation, and cell death in the heart. This was tested in mice only, so it does not show the same would happen in people.
Humanin protein family may help steer cell stress responses
Researchers mapped how Humanin-related proteins connect to other proteins in a computer network. They suggest these proteins may guide stress responses, not just act alone. This is a model, so it does not show these proteins work this way in people.
AGEs-RAGE Axis and Mitochondrial-Derived Peptides in Advanced Chronic Kidney Disease: Interconnected Pathways Beyond Inflammation and Nutrition.
Background. Chronic kidney disease [CKD] is characterized by increased glycoxidative stress, inflammation, and mitochondrial dysfunction.
A humanin analog eased kidney damage in diabetic mice and cells
Researchers found a treated protein reduced kidney damage and cell death in diabetic mice. This work was in mice and cells, so it does not show the same effect in people.
Emerging regulators of human physiology and disease; sORF-encoded microproteins.
The human genome contains hundreds of thousands of short open reading frames (sORFs), yet their translational products, hereafter referred to as sORF-encoded microproteins (also historically termed micropeptides), have…
The MTRNR2L gene family and age-related macular degeneration.
Age-related macular degeneration (AMD) is the leading cause of blindness in aging adults, yet no FDA-approved therapies exist for early and intermediate disease.
