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In the female offspring, mitochondrial fusion markers on P1 suggest increased mitochondrial regeneration, while in adults increased mitochondrial fission and autophagosome markers were observed, with high levels of MnSOD and OXPHOS complex I suggesting an increase in energy demand and oxidative stress, thereby more mitochondrial turnover (Twig et al., In the developing brain, substantially high energy demand increases the need for glucose, oxygen and cerebral blood flow (Hagberg et al., Mitophagy is a crucial process to maintain mitochondrial integrity, where damaged mitochondria can be degraded and the intact components can be recycled to generate new functional mitochondria (Benard and Karbowski, Here in the newborn male SE offspring, both fission and autophagosome markers were increased without changes in the fusion marker, suggesting the mitochondrial damage by maternal SE is irreparable

However, previous reviews emphasize common mechanistic pathways such as inflammation and oxidative stress while emerging pathways particularly autophagy-related signaling are under explored

Medical experts suggest waiting 1 year or more from the onset of symptoms and 3 months witout any evolutivity before having surgery because the course of Peyronies disease is different in each man

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10.1016/0304-4165(90)90088-E [DOI] [PubMed] [Google Scholar] Aroca P., Solano F., Garca-Borrn J