ArticleRedox biology2025
Sex- and age-dependent neurovascular abnormalities linked to neuroinflammation lead to exacerbated post-ischemic brain injury in Marfan syndrome mice.
Article in Redox biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Genetic elastic fiber disorders as neurovascular syndromes: An emerging perspective.Neural regeneration research · 2026Article
- Pain Hypersensitivity in a Mouse Model of Marfan Syndrome.Antioxidants (Basel, Switzerland) · 2026Article
- Inflammatory drivers of carotid atherosclerosis: signaling pathways, immune cells, and plaque stability.Frontiers in cardiovascular medicine · 2026Review
- Apoptosis and Brain Dervived Neurotrophic Factor are increased in cortical neurons of Marfan Syndrome mice.microPublication biology · 2025Article
- Cerebral microvascular density, blood-brain barrier permeability, and support for neuroinflammation indicate early aging in a Marfan syndrome mouse model.Frontiers in physiology · 2024Article
Corrections and comments
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Authors and funding
15 authors.
Funding
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Abstract
Fibrillin 1 gene (Fbn1) mutations cause Marfan syndrome (MFS), triggering life-threatening aortic complications and multi-organ effects. MFS is increasingly linked to neurovascular complications, amplified by aortic surgery risks. However, the impact of MFS on the brain remains unclear, including the roles of sex, aging, and their contribution to cerebral injury. This study examines brain alterations and their role in cerebral ischemic injury in an MFS mouse model. RNA-seq analysis of young (3-month-old) and aged (13-month-old) male and female wild-type and MFS (Fbn1
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