Cross-species evidence for cardiolipin remodeling in neonatal hypoxic–ischemic encephalopathy
knockout mice resulted in accumulation of MLCL and demonstrated larger brain infarct size following HIE in mice, but without affecting mitochondrial respiration or mitochondrial dynamics under basal conditions. These findings suggest that CL remodeling and MLCL accumulation contribute to the progression of neonatal HIE pathology. This study highlights an underexplored mechanism linking cardiolipin remodeling to brain injury severity, offering potential therapeutic targets for neonatal HIE.
Authors
- Katlynn J. Emaus (ORCID: https://orcid.org/0000-0003-2136-6450)
- Erin Gruley
- Thomas H. Sanderson (ORCID: https://orcid.org/0000-0003-0112-8164)
- Francisco J. Torres Torres (ORCID: https://orcid.org/0000-0001-7108-473X)
- Caroline Dubs
- Garrett M. Fogo (ORCID: https://orcid.org/0000-0001-5292-3702)
- Joseph M. Wider (ORCID: https://orcid.org/0000-0002-2859-4846)
- Sarita Raghunayakula
- Reagan L Speas
- Liam McCracken
Institutions
- Brigham and Women's Hospital (US)
- University of Michigan (US)
- University of Colorado Denver (US)
Publication Details
- Journal
- Journal of Cerebral Blood Flow & Metabolism
- Published
- 2026-03-31
- DOI
- https://doi.org/10.1177/0271678x261435368
- Primary Topic
- Mitochondrial Function and Pathology
- Type
- article
- Field-Weighted Citation Impact
- 0.00