Linking LOXL2 to Cardiac Interstitial Fibrosis
Cardiovascular diseases (CVDs) are the leading causes of death worldwide. CVD pathophysiology is often characterized by increased stiffening of the heart muscle due to fibrosis, thus resulting in diminished cardiac function. Fibrosis can be caused by increased oxidative stress and inflammation, whic...
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| Format: | Article |
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MDPI AG
2020-08-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/21/16/5913 |
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| author | Melisse Erasmus Ebrahim Samodien Sandrine Lecour Martin Cour Oscar Lorenzo Phiwayinkosi Dludla Carmen Pheiffer Rabia Johnson |
| author_facet | Melisse Erasmus Ebrahim Samodien Sandrine Lecour Martin Cour Oscar Lorenzo Phiwayinkosi Dludla Carmen Pheiffer Rabia Johnson |
| author_sort | Melisse Erasmus |
| collection | DOAJ |
| description | Cardiovascular diseases (CVDs) are the leading causes of death worldwide. CVD pathophysiology is often characterized by increased stiffening of the heart muscle due to fibrosis, thus resulting in diminished cardiac function. Fibrosis can be caused by increased oxidative stress and inflammation, which is strongly linked to lifestyle and environmental factors such as diet, smoking, hyperglycemia, and hypertension. These factors can affect gene expression through epigenetic modifications. Lysyl oxidase like 2 (LOXL2) is responsible for collagen and elastin cross-linking in the heart, and its dysregulation has been pathologically associated with increased fibrosis. Additionally, studies have shown that, LOXL2 expression can be regulated by DNA methylation and histone modification. However, there is a paucity of data on LOXL2 regulation and its role in CVD. As such, this review aims to gain insight into the mechanisms by which LOXL2 is regulated in physiological conditions, as well as determine the downstream effectors responsible for CVD development. |
| first_indexed | 2024-03-10T17:17:07Z |
| format | Article |
| id | doaj.art-4d379b1959744d5a9e5833f72a549eb2 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-10T17:17:07Z |
| publishDate | 2020-08-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-4d379b1959744d5a9e5833f72a549eb22023-11-20T10:27:23ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672020-08-012116591310.3390/ijms21165913Linking LOXL2 to Cardiac Interstitial FibrosisMelisse Erasmus0Ebrahim Samodien1Sandrine Lecour2Martin Cour3Oscar Lorenzo4Phiwayinkosi Dludla5Carmen Pheiffer6Rabia Johnson7Biomedical Research and Innovation Platform, South African Medical Research Council, Cape Town 7501, South AfricaBiomedical Research and Innovation Platform, South African Medical Research Council, Cape Town 7501, South AfricaHatter Institute for Cardiovascular Research in Africa (HICRA), University of Cape Town, Cape Town 7925, South AfricaHospices Civils de Lyon, Hôpital Edouard Herriot, Service de Médecine Intensive-Réanimation, Place d’Arsonval, 69437 Lyon, FranceInstitute de Investigación Sanitaria-FJD, Faculty of Medicine, University Autónoma de Madrid, 28049 Madrid, SpainBiomedical Research and Innovation Platform, South African Medical Research Council, Cape Town 7501, South AfricaBiomedical Research and Innovation Platform, South African Medical Research Council, Cape Town 7501, South AfricaBiomedical Research and Innovation Platform, South African Medical Research Council, Cape Town 7501, South AfricaCardiovascular diseases (CVDs) are the leading causes of death worldwide. CVD pathophysiology is often characterized by increased stiffening of the heart muscle due to fibrosis, thus resulting in diminished cardiac function. Fibrosis can be caused by increased oxidative stress and inflammation, which is strongly linked to lifestyle and environmental factors such as diet, smoking, hyperglycemia, and hypertension. These factors can affect gene expression through epigenetic modifications. Lysyl oxidase like 2 (LOXL2) is responsible for collagen and elastin cross-linking in the heart, and its dysregulation has been pathologically associated with increased fibrosis. Additionally, studies have shown that, LOXL2 expression can be regulated by DNA methylation and histone modification. However, there is a paucity of data on LOXL2 regulation and its role in CVD. As such, this review aims to gain insight into the mechanisms by which LOXL2 is regulated in physiological conditions, as well as determine the downstream effectors responsible for CVD development.https://www.mdpi.com/1422-0067/21/16/5913Lysyl Oxidase-Like 2 (LOXL2)epigeneticsDNA methylationfibrosiscardiovascular disease (CVD) |
| spellingShingle | Melisse Erasmus Ebrahim Samodien Sandrine Lecour Martin Cour Oscar Lorenzo Phiwayinkosi Dludla Carmen Pheiffer Rabia Johnson Linking LOXL2 to Cardiac Interstitial Fibrosis International Journal of Molecular Sciences Lysyl Oxidase-Like 2 (LOXL2) epigenetics DNA methylation fibrosis cardiovascular disease (CVD) |
| title | Linking LOXL2 to Cardiac Interstitial Fibrosis |
| title_full | Linking LOXL2 to Cardiac Interstitial Fibrosis |
| title_fullStr | Linking LOXL2 to Cardiac Interstitial Fibrosis |
| title_full_unstemmed | Linking LOXL2 to Cardiac Interstitial Fibrosis |
| title_short | Linking LOXL2 to Cardiac Interstitial Fibrosis |
| title_sort | linking loxl2 to cardiac interstitial fibrosis |
| topic | Lysyl Oxidase-Like 2 (LOXL2) epigenetics DNA methylation fibrosis cardiovascular disease (CVD) |
| url | https://www.mdpi.com/1422-0067/21/16/5913 |
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