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, Ca; Khera, Av; Natarajan, P; Klarin, D; Won, Hh; Peloso, Gm; Stitziel, No; Nomura, A; Zekavat, Sm; Bick, Ag; Gupta, N; Asselta, R; Duga, S; Merlini, Pa; Correa, A; Kessler, T; Wilson, Jg; Bown, Mj; Hall, As; Braund, Ps; Samani, Nj; Schunkert, H; Marrugat, J; Elosua, R; Mcpherson, R; Farrall, M; Watkins, H; Willer, C; Abecasis, Gr; Felix, Jf; Vasan, Rs; Lander, E; Rader, Dj; Danesh, J; Ardissino, D; Gabriel, S; Saleheen, D; Kathiresan, S; CHARGE–Heart Failure, Consortium; CARDIoGRAM Exome, Consortium. - 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, Ca; Khera, Av; Natarajan, P; Klarin, D; Won, Hh; Peloso, Gm; Stitziel, No; Nomura, A; Zekavat, Sm; Bick, Ag; Gupta, N; Asselta, R; Duga, S; Merlini, Pa; Correa, A; Kessler, T; Wilson, Jg; Bown, Mj; Hall, As; Braund, Ps; Samani, Nj; Schunkert, H; Marrugat, J; Elosua, R; Mcpherson, R; Farrall, M; Watkins, H; Willer, C; Abecasis, Gr; Felix, Jf; Vasan, Rs; Lander, E; Rader, Dj; Danesh, J; Ardissino, D; Gabriel, S; Saleheen, D; Kathiresan, S; CHARGE–Heart Failure, Consortium; CARDIoGRAM Exome, Consortium. - 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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