The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
The Permeability Transition Pore Controls Cardiac Mitochondrial Maturation and Myocyte Differentiation
Open accessAbstract
SUMMARY Although mature myocytes rely on mitochondria as the primary source of energy, the role of mitochondria in the developing heart is not well known. Here, we find closure of the mitochondrial permeability transition pore (mPTP) drives maturation of mitochondrial structure and function and myocyte differentiation. Cardiomyocytes at embryonic day (E) 9.5, when compared to E13.5, displayed fragmented mitochondria with few cristae, a less polarized mitochondrial membrane potential, higher reactive oxygen species (ROS) levels, and an open mPTP. Pharmacologic and genetic closing of the mPTP yielded maturation of mitochondrial structure and function, lowered ROS, and increased myocyte differentiation (measured by counting Z-bands). Furthermore, myocyte differentiation was inhibited and enhanced with oxidant and antioxidant treatment, respectively, suggesting that redox signaling pathways lie downstream of mitochondria to regulate cardiac myocyte differentiation.
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Cites
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Self-citationThe mitochondrial permeability transition pore and its role in cell death
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“Although it was initially reported that CyP-D null mice have no cardiac phenotype and survive gestation and have a normal lifespan (Baines et al., 2005; Basso et al., 2005; Nakagawa et al., 2005), we observed “premature” mitochondrial maturation and myocyte differentiation in E9.”
Properties of the Permeability Transition Pore in Mitochondria Devoid of Cyclophilin D
Basso, E., Fante, L., Fowlkes, J., Petronilli, V., Forte, M. A., & Bernardi, P. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.c500089200 · Cited by 808 · cited 2×
“The mPTP is defined by its inhibition by Cyclosporin A (CsA), an immunosuppressant that binds to mitochondrial CyP-D to block the calcium ion-induced permeability transition (Basso et al, 2005; Friberg et al, 1998).”
Superoxide flashes in single mitochondria
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Self-citationMitochondrial filaments and clusters as intracellular power-transmitting cables
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Self-citationCaspase-cleaved Tau Expression Induces Mitochondrial Dysfunction in Immortalized Cortical Neurons
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Self-citationBioenergetics, mitochondria, and cardiac myocyte differentiation
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Cited by
ROS function in redox signaling and oxidative stress
Schieber, M., & Chandel, N. S. (2014) · Current Biology · doi:10.1016/j.cub.2014.03.034 · Cited by 6,931
Engineering Adolescence: Maturation of Human Pluripotent Stem Cell–Derived Cardiomyocytes
Yang, X., Pabon, L., & Murry, C. E. (2014) · Circulation Research · doi:10.1161/circresaha.114.300558 · Cited by 939
Mitochondrial Cristae: Where Beauty Meets Functionality
Cogliati, S., Enriquez, J. A., & Scorrano, L. (2016) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2016.01.001 · Cited by 816
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Stem cells and the impact of ROS signaling
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Metadata
- Authors
- Hom, J. R., Quintanilla, R. A., Hoffman, D. L., de Mesy Bentley, K. L., Molkentin, J. D., Sheu, S.-S., & Porter, G. A.
- Venue
- Developmental Cell
- Publisher
- Elsevier BV
- Published
- 2011-09
- Volume
- 21
- Issue
- 3
- Pages
- 469-478
- ISSN
- 1534-5807 (ISSN-L)
- OpenAlex
- W2082973248
- Cited by
- 299
- References
- 10
- FWCI
- 6.47
- Type
- journal article
- Language
- en
- Open access
- bronze
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