ArticlePloS one2025
SS-31: A promising therapeutic agent against bleomycin-induced pulmonary fibrosis in Mice.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Elamipretide Rejuvenates Oocyte Quality and Restores Female Fertility During Reproductive Aging.Aging cell · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe aim of this research was to investigate if the mitochondria- targeting peptide SS-31 could serve as a protective measure against bleomycin-induced pulmonary fibrosis in mice.
methodMice were split into four groups named CON group, SS-31 group, BLM group, and the BLM + SS-31 group. SS-31 (intraperitoneal injection, 5mg/Kg) was administered daily from the day prior to the experiment for the control and model groups. Mice were euthanized after 28 days of the experiment, following which blood, bronchoalveolar lavage fluid, and lung tissue were collected for analysis.
resultsBLM caused a large decrease in body weight in mice. However, the intraperitoneal injection of SS-31 slowed down the body weight loss in the mice. It was observed through HE and Masson staining, immunohistochemistry, hydroxyproline detection, and fibrosis index measurement via Western blot that SS-31 could alleviate pulmonary fibrosis caused by BLM. Electron microscopy and ATP detection further suggested that SS-31 might help protect mitochondrial structure and function. It was also found that SS-31 could reduce reactive oxygen species and myeloperoxidase, thereby alleviating the reduction of antioxidant factor MPO and SOD, as well as diminishing the inflammatory factors TNF-α, IL-1 β, and IL-6.
conclusionThe mitochondria-targeting drug SS-31 exhibited potential in mitigating bleomycin-induced pulmonary fibrosis, improving mitochondrial structural and functional damage, stabilizing the balance between oxidative and antioxidant systems, reducing inflammatory factor expression, and improving apoptosis in lung tissue.
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