Author

P. H. Backx

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Bioengineering· 1 Cell Biology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:clustering· 1 Approach:deep learning· 1 Research Focus:differential expression· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

J. A. Simpson· 2 shared A. Brahmbhatt· 1 shared A. O. Gramolini· 1 shared B. G. Neel· 1 shared C. A. Simmons· 1 shared C. G. R. Perry· 1 shared E. Y. Wang· 1 shared F. Billia· 1 shared

Activity by Year

2017-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 16 mutual co-author links

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2 shared papersPhysiology

J. A. Simpson

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Author profile →

3 papers

Recent·Most cited

Disrupted cardiac bioenergetics linked to oxidized mitochondrial creatine kinase are rescued by the mitochondrial-targeting peptide SBT-20 in the D2.mdx model of Duchenne muscular dystrophy

C. G. R. Perry, M. C. Hughes, S. V. Ramos, A. Brahmbhatt, P. C. Turnbull, N. Polidovitch, M. C. Garibotti, U. Schlattner, T. J. Hawke, J. A. Simpson, P. H. Backx

This paper investigates how mitochondrial bioenergetics are affected in D2.mdx mice and shows that SBT-20 can improve creatine-dependent bioenergetics by reducing oxidative stress.

bioRxiv · Feb 4, 2024 · PreprintPhysiology

Advanced physiological maturation of iPSC-derived human cardiomyocytes using an algorithm-directed optimization of defined media components

N. I. Callaghan, L. J. Durland, W. Chen, U. Kuzmanov, M. Z. Miranda, Z. Mirzaei, R. G. Ireland, E. Y. Wang, K. Wagner, M. M. Kim, J. Audet, P. Santerre, A. O. Gramolini, F. Billia, M. Radisic, , C. A. Simmons

This study develops a novel medium for iPSC-derived cardiomyocytes using differential evolution to enhance maturation, validated through multiomic analysis.

bioRxiv · Oct 10, 2022Bioengineering

Cellular Interplay and Cytokine Hierarchy Cause Pathological Cardiac Hypertrophy in RAF1-Mutant Noonan Syndrome

J. C. Yin, M. J. Platt, X. Tian, X. Wu, P. H. Backx, J. A. Simpson, T. Araki, B. G. Neel

This study shows that RAF1 mutations in Noonan syndrome cause cardiac hypertrophy through cytokine signaling from endothelial cells, with TNF/IL6 as potential therapeutic targets.

bioRxiv · Mar 30, 2017Cell Biology