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For:	Koleini N, Nickel BE, Nagalingam RS, Landry NM, Fandrich RR, Cheung DYC, Dixon IM, Czubryt MP, Jassal DS, Cattini PA, Kardami E. Elimination of endogenous high molecular weight FGF2 prevents pressure-overload-induced systolic dysfunction, linked to increased FGFR1 activity and NR1D1 expression. Cell Tissue Res 2021. [PMID: 34057573 DOI: 10.1007/s00441-021-03465-0] [Cited by in F6Publishing: 1] [Reference Citation Analysis]

For:

Koleini N, Nickel BE, Nagalingam RS, Landry NM, Fandrich RR, Cheung DYC, Dixon IM, Czubryt MP, Jassal DS, Cattini PA, Kardami E. Elimination of endogenous high molecular weight FGF2 prevents pressure-overload-induced systolic dysfunction, linked to increased FGFR1 activity and NR1D1 expression. Cell Tissue Res 2021. [PMID: 34057573 DOI: 10.1007/s00441-021-03465-0] [Cited by in F6Publishing: 1] [Reference Citation Analysis]

Number	Citing Articles
1	Ornitz DM, Itoh N. New developments in the biology of fibroblast growth factors. WIREs Mech Dis 2022;:e1549. [PMID: 35142107 DOI: 10.1002/wsbm.1549] [Reference Citation Analysis]
2	Srisakuldee W, Nickel BE, Fandrich RR, Zhang F, Pasumarthi KBS, Kardami E. A Cardiac Mitochondrial FGFR1 Mediates the Antithetical Effects of FGF2 Isoforms on Permeability Transition. Cells 2021;10:2735. [PMID: 34685716 DOI: 10.3390/cells10102735] [Reference Citation Analysis]