Genomic analyses have suggested that the LPA gene and its associated plasma biomarker, lipoprotein(a) (Lp[a]), represent a causal risk factor for coronary heart disease (CHD). As such, lowering Lp(a) has emerged as a therapeutic strategy. Beyond target identification, human genetics may contribute to the development of new therapies by defining the full spectrum of beneficial and adverse consequences and by developing a dose-response curve of target perturbation.

Phenotypic Characterization of Genetically Lowered Human Lipoprotein(a) Levels / Emdin, C.a., Khera, A.v., Natarajan, P., Klarin, D., Won, H.h., Peloso, G.m., Stitziel, N.o., Nomura, A., Zekavat, S.m., Bick, A.g., Gupta, N., Asselta, R., Duga, S., Merlini, P.a., Correa, A., Kessler, T., Wilson, J.g., Bown, M.j., Hall, A.s., Braund, P.s., et al.. - 68:(2016), pp. 2761-2772. [10.1016/j.jacc.2016.10.033]

Phenotypic Characterization of Genetically Lowered Human Lipoprotein(a) Levels

Ardissino D;
2016-01-01

Abstract

Genomic analyses have suggested that the LPA gene and its associated plasma biomarker, lipoprotein(a) (Lp[a]), represent a causal risk factor for coronary heart disease (CHD). As such, lowering Lp(a) has emerged as a therapeutic strategy. Beyond target identification, human genetics may contribute to the development of new therapies by defining the full spectrum of beneficial and adverse consequences and by developing a dose-response curve of target perturbation.
2016
Phenotypic Characterization of Genetically Lowered Human Lipoprotein(a) Levels / Emdin, C.a., Khera, A.v., Natarajan, P., Klarin, D., Won, H.h., Peloso, G.m., Stitziel, N.o., Nomura, A., Zekavat, S.m., Bick, A.g., Gupta, N., Asselta, R., Duga, S., Merlini, P.a., Correa, A., Kessler, T., Wilson, J.g., Bown, M.j., Hall, A.s., Braund, P.s., et al.. - 68:(2016), pp. 2761-2772. [10.1016/j.jacc.2016.10.033]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11381/2883791
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