HDL as Bidirectional Lipid Vectors: Time for New Paradigms
The anti-atherogenic properties of high-density lipoproteins (HDL) have been explained mainly by reverse cholesterol transport (RCT) from peripheral tissues to the liver. The RCT seems to agree with most of the negative epidemiological correlations between HDL cholesterol levels and coronary artery...
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| Format: | Article |
| Language: | English |
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MDPI AG
2022-05-01
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| Series: | Biomedicines |
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| Online Access: | https://www.mdpi.com/2227-9059/10/5/1180 |
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| author | María Luna-Luna Eric Niesor Óscar Pérez-Méndez |
| author_facet | María Luna-Luna Eric Niesor Óscar Pérez-Méndez |
| author_sort | María Luna-Luna |
| collection | DOAJ |
| description | The anti-atherogenic properties of high-density lipoproteins (HDL) have been explained mainly by reverse cholesterol transport (RCT) from peripheral tissues to the liver. The RCT seems to agree with most of the negative epidemiological correlations between HDL cholesterol levels and coronary artery disease. However, therapies designed to increase HDL cholesterol failed to reduce cardiovascular risk, despite their capacity to improve cholesterol efflux, the first stage of RCT. Therefore, the cardioprotective role of HDL may not be explained by RCT, and it is time for new paradigms about the physiological function of these lipoproteins. It should be considered that the main HDL apolipoprotein, apo AI, has been highly conserved throughout evolution. Consequently, these lipoproteins play an essential physiological role beyond their capacity to protect against atherosclerosis. We propose HDL as bidirectional lipid vectors carrying lipids from and to tissues according to their local context. Lipid influx mediated by HDL appears to be particularly important for tissue repair right on site where the damage occurs, including arteries during the first stages of atherosclerosis. In contrast, the HDL-lipid efflux is relevant for secretory cells where the fusion of intracellular vesicles drastically enlarges the cytoplasmic membrane with the potential consequence of impairment of cell function. In such circumstances, HDL could deliver some functional lipids and pick up not only cholesterol but an integral part of the membrane in excess, restoring the viability of the secretory cells. This hypothesis is congruent with the beneficial effects of HDL against atherosclerosis as well as with their capacity to induce insulin secretion and merits experimental exploration. |
| first_indexed | 2024-03-10T03:16:19Z |
| format | Article |
| id | doaj.art-31b1f1f8fc2647219ba2aa41c008ab73 |
| institution | Directory Open Access Journal |
| issn | 2227-9059 |
| language | English |
| last_indexed | 2024-03-10T03:16:19Z |
| publishDate | 2022-05-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Biomedicines |
| spelling | doaj.art-31b1f1f8fc2647219ba2aa41c008ab732023-11-23T10:12:13ZengMDPI AGBiomedicines2227-90592022-05-01105118010.3390/biomedicines10051180HDL as Bidirectional Lipid Vectors: Time for New ParadigmsMaría Luna-Luna0Eric Niesor1Óscar Pérez-Méndez2Department of Molecular Biology, Instituto Nacional de Cardiología “Ignacio Chávez”, Mexico City 14080, MexicoHartis Pharma, 13C Chemin de Bonmont, 1260 Nyon, SwitzerlandDepartment of Molecular Biology, Instituto Nacional de Cardiología “Ignacio Chávez”, Mexico City 14080, MexicoThe anti-atherogenic properties of high-density lipoproteins (HDL) have been explained mainly by reverse cholesterol transport (RCT) from peripheral tissues to the liver. The RCT seems to agree with most of the negative epidemiological correlations between HDL cholesterol levels and coronary artery disease. However, therapies designed to increase HDL cholesterol failed to reduce cardiovascular risk, despite their capacity to improve cholesterol efflux, the first stage of RCT. Therefore, the cardioprotective role of HDL may not be explained by RCT, and it is time for new paradigms about the physiological function of these lipoproteins. It should be considered that the main HDL apolipoprotein, apo AI, has been highly conserved throughout evolution. Consequently, these lipoproteins play an essential physiological role beyond their capacity to protect against atherosclerosis. We propose HDL as bidirectional lipid vectors carrying lipids from and to tissues according to their local context. Lipid influx mediated by HDL appears to be particularly important for tissue repair right on site where the damage occurs, including arteries during the first stages of atherosclerosis. In contrast, the HDL-lipid efflux is relevant for secretory cells where the fusion of intracellular vesicles drastically enlarges the cytoplasmic membrane with the potential consequence of impairment of cell function. In such circumstances, HDL could deliver some functional lipids and pick up not only cholesterol but an integral part of the membrane in excess, restoring the viability of the secretory cells. This hypothesis is congruent with the beneficial effects of HDL against atherosclerosis as well as with their capacity to induce insulin secretion and merits experimental exploration.https://www.mdpi.com/2227-9059/10/5/1180apolipoprotein AIdiabetes mellitussphingomyelincholesterolwound healingendothelial cell |
| spellingShingle | María Luna-Luna Eric Niesor Óscar Pérez-Méndez HDL as Bidirectional Lipid Vectors: Time for New Paradigms Biomedicines apolipoprotein AI diabetes mellitus sphingomyelin cholesterol wound healing endothelial cell |
| title | HDL as Bidirectional Lipid Vectors: Time for New Paradigms |
| title_full | HDL as Bidirectional Lipid Vectors: Time for New Paradigms |
| title_fullStr | HDL as Bidirectional Lipid Vectors: Time for New Paradigms |
| title_full_unstemmed | HDL as Bidirectional Lipid Vectors: Time for New Paradigms |
| title_short | HDL as Bidirectional Lipid Vectors: Time for New Paradigms |
| title_sort | hdl as bidirectional lipid vectors time for new paradigms |
| topic | apolipoprotein AI diabetes mellitus sphingomyelin cholesterol wound healing endothelial cell |
| url | https://www.mdpi.com/2227-9059/10/5/1180 |
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