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Sortilin, Encoded by the Cardiovascular Risk Gene SORT1, and Its Suggested Functions in Cardiovascular Disease

  • Genetics (AJ Marian, Section Editor)
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Abstract

Several genome-wide association studies have linked novel loci to a wide range of cardiovascular phenotypes including low-density lipoprotein (LDL)-cholesterol, early onset myocardial infarction, coronary artery calcification, coronary artery stenosis, and abdominal aorta aneurysm. Especially, one locus, namely, 1p13.3, has attracted much attention. This locus harbors four candidate genes, CELSR2, PSRC1, MYBPHL, and SORT1. SORT1 encodes sortilin, a type I sorting receptor that has recently been implicated in LDL-cholesterol metabolism, VLDL secretion, PCSK9 secretion, and development of atherosclerotic lesions. Furthermore, sortilin also seems to be involved in the development of atherosclerosis, by mechanisms not directly involving LDL-cholesterol, but possibly resulting from the attenuated secretion of proinflammatory cytokines, such as IL6 and TNFα, which accompanies lack of sortilin in immune cells. Sortilin seems to play an important role in the development of cardiovascular disease and have functions beyond regulating LDL-cholesterol.

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Notes

  1. The sortilin cytoplasmic tail conveys Golgi-endosome trafficking [43], and previous studies have suggested that sortilin binds a number of lysosomal enzymes in the biosynthetic pathway and mediates their transport to the lysosomes (e.g., [52]). However, other sortilin ligands like lipoprotein lipase are apparently not targeted directly from the TGN [37] to the lysosomes [53] and, notably, sortilin deficient mice show no signs of lysosomal storage disease. Whether sortilin actually serves in TGN-endosomal/lysosomal protein-transport is therefore still an open question.

  2. The sortilin-deficient mouse employed by Kjolby et al. expresses a truncated, misfolded version of sortilin which is incapable of ligand-linding and never leaves the ER. The mouse is therefore in effect a functional knockout [6, 56].

  3. Musunuru et al. [7] stated an almost 60 percent increase of total cholesterol in sortilin knockouts compared to wildtype animals, whereas Strong et al. [61••] reported a 20 percent decrease using the same sortili- deficient mice on Ldlr knockout background, which is in agreement with findings by Kjolby et al. [6].

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Acknowledgments

Authors are funded by The Danish Diabetes Academy supported by the Novo Nordisk Foundation (MFK), and The Lundbeck Foundation (MFK, CMP, MSN).

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Mads Kjolby, Morten Schallburg Nielsen, and Claus Munck Petersen declare that they have no conflict of interest.

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This article does not contain any studies with human or animal subjects performed by any of the authors.

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Authors and Affiliations

  1. Lundbeck Foundation Research Centre MIND, Aarhus University, Aarhus, Denmark

    Mads Kjolby, Morten Schallburg Nielsen & Claus Munck Petersen

  2. Danish Diabetes Academy, Odense, Denmark

    Mads Kjolby

  3. Danish Research Institute of Translational Neuroscience, Nordic EMBL Partnership for Molecular Medicine, Aarhus, Denmark

    Mads Kjolby

  4. Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark

    Mads Kjolby

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  1. Mads Kjolby
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Kjolby, M., Nielsen, M.S. & Petersen, C.M. Sortilin, Encoded by the Cardiovascular Risk Gene SORT1, and Its Suggested Functions in Cardiovascular Disease. Curr Atheroscler Rep 17, 18 (2015). https://doi.org/10.1007/s11883-015-0496-7

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