Increased Remnant Lipoproteins in Apo E Deficient Mice Induce Coronary Atherosclerosis following Transverse Aortic Constriction and Aggravate the Development of Pressure Overload-Induced Cardiac Hypertrophy and Heart Failure
Murine coronary arteries are very resistant to the development of atherosclerosis, which may be related to their intramyocardial course. Blood pressure promotes atherosclerotic plaque formation by acting as a physical force that potentiates the migration of pro-atherogenic lipoproteins across the en...
| Main Authors: | , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2022-07-01
|
| Series: | Biomedicines |
| Subjects: | |
| Online Access: | https://www.mdpi.com/2227-9059/10/7/1592 |
| _version_ | 1797440691332186112 |
|---|---|
| author | Ilayaraja Muthuramu Mudit Mishra Bart De Geest |
| author_facet | Ilayaraja Muthuramu Mudit Mishra Bart De Geest |
| author_sort | Ilayaraja Muthuramu |
| collection | DOAJ |
| description | Murine coronary arteries are very resistant to the development of atherosclerosis, which may be related to their intramyocardial course. Blood pressure promotes atherosclerotic plaque formation by acting as a physical force that potentiates the migration of pro-atherogenic lipoproteins across the endothelium. C57BL/6N apolipoprotein (apo) E deficient mice have increased remnant lipoproteins that are a risk factor for coronary atherosclerosis. In this study, our aim was to quantify coronary atherosclerosis and artery remodeling following transverse aortic constriction (TAC) in C57BL/6N apo E<sup>−/−</sup> mice and to evaluate the impact of increased remnant lipoproteins on the development of pressure overload-induced cardiac hypertrophy and heart failure. Advanced atherosclerotic lesions were observed in the left coronary artery of C57BL/6N apo E<sup>−/−</sup> TAC mice but not in C57BL/6N TAC mice. Pressure overload resulted in markedly increased cardiac hypertrophy and more pronounced heart failure in C57BL/6N apo E<sup>−/−</sup> TAC mice in comparison to C57BL/6N TAC mice. Pathological hypertrophy, as evidenced by increased myocardial fibrosis and capillary rarefaction, was more prominent in C57BL/6N TAC apo E<sup>−/−</sup> than in C57BL/6N TAC mice and led to more marked cardiac dysfunction. In conclusion, TAC in apo E deficient mice induces coronary atherosclerosis and aggravates the development of pathological cardiac hypertrophy and heart failure. |
| first_indexed | 2024-03-09T12:13:03Z |
| format | Article |
| id | doaj.art-9ccf042b7b0a4c6b96c7ca01c581549f |
| institution | Directory Open Access Journal |
| issn | 2227-9059 |
| language | English |
| last_indexed | 2024-03-09T12:13:03Z |
| publishDate | 2022-07-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Biomedicines |
| spelling | doaj.art-9ccf042b7b0a4c6b96c7ca01c581549f2023-11-30T22:50:34ZengMDPI AGBiomedicines2227-90592022-07-01107159210.3390/biomedicines10071592Increased Remnant Lipoproteins in Apo E Deficient Mice Induce Coronary Atherosclerosis following Transverse Aortic Constriction and Aggravate the Development of Pressure Overload-Induced Cardiac Hypertrophy and Heart FailureIlayaraja Muthuramu0Mudit Mishra1Bart De Geest2Centre for Molecular and Vascular Biology, Catholic University of Leuven, 3000 Leuven, BelgiumCentre for Molecular and Vascular Biology, Catholic University of Leuven, 3000 Leuven, BelgiumCentre for Molecular and Vascular Biology, Catholic University of Leuven, 3000 Leuven, BelgiumMurine coronary arteries are very resistant to the development of atherosclerosis, which may be related to their intramyocardial course. Blood pressure promotes atherosclerotic plaque formation by acting as a physical force that potentiates the migration of pro-atherogenic lipoproteins across the endothelium. C57BL/6N apolipoprotein (apo) E deficient mice have increased remnant lipoproteins that are a risk factor for coronary atherosclerosis. In this study, our aim was to quantify coronary atherosclerosis and artery remodeling following transverse aortic constriction (TAC) in C57BL/6N apo E<sup>−/−</sup> mice and to evaluate the impact of increased remnant lipoproteins on the development of pressure overload-induced cardiac hypertrophy and heart failure. Advanced atherosclerotic lesions were observed in the left coronary artery of C57BL/6N apo E<sup>−/−</sup> TAC mice but not in C57BL/6N TAC mice. Pressure overload resulted in markedly increased cardiac hypertrophy and more pronounced heart failure in C57BL/6N apo E<sup>−/−</sup> TAC mice in comparison to C57BL/6N TAC mice. Pathological hypertrophy, as evidenced by increased myocardial fibrosis and capillary rarefaction, was more prominent in C57BL/6N TAC apo E<sup>−/−</sup> than in C57BL/6N TAC mice and led to more marked cardiac dysfunction. In conclusion, TAC in apo E deficient mice induces coronary atherosclerosis and aggravates the development of pathological cardiac hypertrophy and heart failure.https://www.mdpi.com/2227-9059/10/7/1592coronary atherosclerosispathological hypertrophyheart failureapolipoprotein Eremnant lipoproteinsoxidative stress |
| spellingShingle | Ilayaraja Muthuramu Mudit Mishra Bart De Geest Increased Remnant Lipoproteins in Apo E Deficient Mice Induce Coronary Atherosclerosis following Transverse Aortic Constriction and Aggravate the Development of Pressure Overload-Induced Cardiac Hypertrophy and Heart Failure Biomedicines coronary atherosclerosis pathological hypertrophy heart failure apolipoprotein E remnant lipoproteins oxidative stress |
| title | Increased Remnant Lipoproteins in Apo E Deficient Mice Induce Coronary Atherosclerosis following Transverse Aortic Constriction and Aggravate the Development of Pressure Overload-Induced Cardiac Hypertrophy and Heart Failure |
| title_full | Increased Remnant Lipoproteins in Apo E Deficient Mice Induce Coronary Atherosclerosis following Transverse Aortic Constriction and Aggravate the Development of Pressure Overload-Induced Cardiac Hypertrophy and Heart Failure |
| title_fullStr | Increased Remnant Lipoproteins in Apo E Deficient Mice Induce Coronary Atherosclerosis following Transverse Aortic Constriction and Aggravate the Development of Pressure Overload-Induced Cardiac Hypertrophy and Heart Failure |
| title_full_unstemmed | Increased Remnant Lipoproteins in Apo E Deficient Mice Induce Coronary Atherosclerosis following Transverse Aortic Constriction and Aggravate the Development of Pressure Overload-Induced Cardiac Hypertrophy and Heart Failure |
| title_short | Increased Remnant Lipoproteins in Apo E Deficient Mice Induce Coronary Atherosclerosis following Transverse Aortic Constriction and Aggravate the Development of Pressure Overload-Induced Cardiac Hypertrophy and Heart Failure |
| title_sort | increased remnant lipoproteins in apo e deficient mice induce coronary atherosclerosis following transverse aortic constriction and aggravate the development of pressure overload induced cardiac hypertrophy and heart failure |
| topic | coronary atherosclerosis pathological hypertrophy heart failure apolipoprotein E remnant lipoproteins oxidative stress |
| url | https://www.mdpi.com/2227-9059/10/7/1592 |
| work_keys_str_mv | AT ilayarajamuthuramu increasedremnantlipoproteinsinapoedeficientmiceinducecoronaryatherosclerosisfollowingtransverseaorticconstrictionandaggravatethedevelopmentofpressureoverloadinducedcardiachypertrophyandheartfailure AT muditmishra increasedremnantlipoproteinsinapoedeficientmiceinducecoronaryatherosclerosisfollowingtransverseaorticconstrictionandaggravatethedevelopmentofpressureoverloadinducedcardiachypertrophyandheartfailure AT bartdegeest increasedremnantlipoproteinsinapoedeficientmiceinducecoronaryatherosclerosisfollowingtransverseaorticconstrictionandaggravatethedevelopmentofpressureoverloadinducedcardiachypertrophyandheartfailure |