H
Hanna Osinska
Researcher at Cincinnati Children's Hospital Medical Center
Publications - 84
Citations - 9231
Hanna Osinska is an academic researcher from Cincinnati Children's Hospital Medical Center. The author has contributed to research in topics: Cardiomyopathy & Desmin. The author has an hindex of 44, co-authored 83 publications receiving 8515 citations. Previous affiliations of Hanna Osinska include University of Cincinnati & Hospital Research Foundation.
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Journal ArticleDOI
Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death
Christopher P. Baines,Robert A. Kaiser,Nicole H. Purcell,N. Scott Blair,Hanna Osinska,Michael Hambleton,Eric W. Brunskill,M. Richard Sayen,Roberta A. Gottlieb,Gerald W. Dorn,Jeffrey Robbins,Jeffery D. Molkentin +11 more
TL;DR: Cyclophilin D and the mitochondrial permeability transition are required for mediating Ca2+- and oxidative damage-induced cell death, but not Bcl-2 family member-regulated death.
Journal ArticleDOI
Extracellular Matrix Remodeling and Organization in Developing and Diseased Aortic Valves
Robert B. Hinton,Joy Lincoln,Gail H. Deutsch,Hanna Osinska,Peter B. Manning,D. Woodrow Benson,Katherine E. Yutzey +6 more
TL;DR: These studies show that normal valve development is characterized by spatiotemporal coordination of ECM organization and VIC compartmentalization and that these developmental processes are disrupted in pediatric patients with diseased BAVs.
Journal ArticleDOI
Genetic and pharmacologic inhibition of mitochondrial-dependent necrosis attenuates muscular dystrophy
Douglas P. Millay,Michelle A. Sargent,Hanna Osinska,Christopher P. Baines,Elisabeth R. Barton,Grégoire Vuagniaux,H. Lee Sweeney,Jeffrey Robbins,Jeffery D. Molkentin +8 more
TL;DR: It is shown that deletion of the gene encoding cyclophilin D rendered mitochondria largely insensitive to the calcium overload–induced swelling associated with a defective sarcolemma, thus reducing myofiber necrosis in two distinct models of muscular dystrophy.
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Expression of R120G–αB-Crystallin Causes Aberrant Desmin and αB-Crystallin Aggregation and Cardiomyopathy in Mice
Xuejun Wang,Hanna Osinska,Raisa Klevitsky,A. Martin Gerdes,Michelle L. Nieman,John N. Lorenz,Timothy E. Hewett,Jeffrey Robbins +7 more
TL;DR: Overexpression of wild-type CryAB was relatively benign, with no increases in mortality and no induction of desmin-related cardiomyopathy even in a line in which CryAB mRNA expression was increased ≈104-fold and the protein level increased by 11-fold.
Journal ArticleDOI
Desmin-related cardiomyopathy in transgenic mice: a cardiac amyloidosis.
Atsushi Sanbe,Hanna Osinska,Jeffrey E. Saffitz,Charles G. Glabe,Rakez Kayed,Alina Maloyan,Jeffrey Robbins +6 more
TL;DR: It is shown that expression of CryAB(R120G) leads to the formation of electron-dense bodies characteristic of the DRMs and identify these bodies as aggresomes, which are characteristic ofThe neurodegenerative diseases.