Impaired Mitochondrial Function in iPSC-Retinal Pigment Epithelium with the Complement Factor H Polymorphism for Age-Related Macular Degeneration
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Age-related macular degeneration (AMD), the leading cause of vision loss in the elderly, is characterized by loss of the retinal pigment epithelium (RPE). While the disease mechanism remains unclear, prior studies have linked AMD with RPE mitochondrial defects and genetic polymorphisms in the complement pathway. This study used RPE generated from induced pluripotent stem cells (iPSC-RPE), which were derived from human donors with or without AMD and genotyped for the complement factor H (CFH) AMD high-risk allele (rs1061170, Y402H) to investigate whether donor disease state or genotype had a detrimental effect on mitochondrial function and inflammation. Results show that cells derived from donors with AMD display decreased mitochondrial function under conditions of stress and elevated expression of inflammatory markers compared to iPSC-RPE from individuals without AMD. A more pronounced reduction in mitochondrial function and increased inflammatory markers was observed in CFH high-risk cells, irrespective of disease state. These results provide evidence for a previously unrecognized link between CFH and mitochondrial function that could contribute to RPE loss in AMD patients harboring the CFH high-risk genotype.
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Dysfunctional FH, including the p.Y402H variant, can lead to overactivation of the complement system, which can impair the essential functions of RPE cells, including autophagy, lysosomal function, and energy metabolism.
“Dysfunctional FH, including the p.Y402H variant, can also lead to overactivation of the complement system, which can impair the essential functions of RPE cells, including autophagy, lysosomal function, and energy metabolism.”
From Bruch’s Membrane: A Key Consideration with Complement-Based Therapies for Age-Related Macular Degeneration (2023) · cites this paper as [135]
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- Authors
- Ebeling, M. C., Geng, Z., Kapphahn, R. J., Roehrich, H., Montezuma, S. R., Dutton, J. R., & Ferrington, D. A.
- Affiliations
- University of Minnesota (US)
- Corresponding author
- Dutton, James R.
- Ferrington, Deborah A.
- Venue
- Cells
- Publisher
- MDPI AG
- Published
- 2021-04-02
- Volume
- 10
- Issue
- 4
- Pages
- 789
- ISSN
- 2073-4409 (ISSN-L)
- PMC
- PMC8066149
- OpenAlex
- W3147418878
- Cited by
- 51
- References
- 62
- Citations by year
- 2026: 9 · 2025: 8 · 2024: 6 · 2023: 5 · 2022: 17 · 2021: 6
- FWCI
- 7.57
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cells (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (R01EY026012, R01EY0285541, P30EY11374)
- Regenerative Medicine Minnesota (2015-5337, 091717 TR 009)
- Topics
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Retinal Imaging and Analysis
- Keywords
- age-related macular degeneration, retinal pigment epithelium, mitochondrial dysfunction, complement factor H, CFH Y402H polymorphism, rs1061170, inflammation, complement pathway, retinal degeneration
- MeSH terms
- Aged, Aged, 80 and over, Cell Line, Complement System Proteins, Epithelial Cells, Female, Humans, Inflammation, Macular Degeneration, Male, Middle Aged, Mitochondria, Models, Biological, Polymorphism, Genetic, Risk, Tissue Donors, Biomarkers, Complement Factor H, Mitochondrial Proteins, Retinal Pigment Epithelium, Induced Pluripotent Stem Cells
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