Cholesterol lowering depletes atherosclerotic lesions of smooth muscle cell-derived fibromyocytes and chondromyocytes
Drugs that lower plasma apolipoprotein B (ApoB)-containing lipoproteins are central to treating advanced atherosclerosis and provide partial protection against clinical events. Previous research showed that lowering ApoB-containing lipoproteins stops plaque inflammation, but how these drugs affect t...
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| Veröffentlicht in: | Nature Cardiovascular Research 2024-02, Vol.3 (2), p.203-220 |
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| creator | Carramolino, Laura Albarrán-Juárez, Julián Markov, Anton Hernández-SanMiguel, Esther Sharysh, Diana Cumbicus, Vanessa Morales-Cano, Daniel Labrador-Cantarero, Verónica Møller, Peter Loof Nogales, Paula Benguria, Alberto Dopazo, Ana Sanchez-Cabo, Fátima Torroja, Carlos Bentzon, Jacob F |
| description | Drugs that lower plasma apolipoprotein B (ApoB)-containing lipoproteins are central to treating advanced atherosclerosis and provide partial protection against clinical events. Previous research showed that lowering ApoB-containing lipoproteins stops plaque inflammation, but how these drugs affect the heterogeneous population of plaque cells derived from smooth muscle cells (SMCs) is unknown. SMC-derived cells are the main cellular component of atherosclerotic lesions and the source of structural components that determine the size of plaques and their propensity to rupture and trigger thrombosis, the proximate cause of heart attack and stroke. Using lineage tracing and single-cell techniques to investigate the full SMC-derived cellular compartment in progressing and regressing plaques in mice, here we show that lowering ApoB-containing lipoproteins reduces nuclear factor kappa-light-chain-enhancer of activated B cells signaling in SMC-derived fibromyocytes and chondromyocytes and leads to depletion of these abundant cell types from plaques. These results uncover an important mechanism through which cholesterol-lowering drugs can achieve plaque regression. |
| doi_str_mv | 10.1038/s44161-023-00412-w |
| format | Article |
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Previous research showed that lowering ApoB-containing lipoproteins stops plaque inflammation, but how these drugs affect the heterogeneous population of plaque cells derived from smooth muscle cells (SMCs) is unknown. SMC-derived cells are the main cellular component of atherosclerotic lesions and the source of structural components that determine the size of plaques and their propensity to rupture and trigger thrombosis, the proximate cause of heart attack and stroke. Using lineage tracing and single-cell techniques to investigate the full SMC-derived cellular compartment in progressing and regressing plaques in mice, here we show that lowering ApoB-containing lipoproteins reduces nuclear factor kappa-light-chain-enhancer of activated B cells signaling in SMC-derived fibromyocytes and chondromyocytes and leads to depletion of these abundant cell types from plaques. These results uncover an important mechanism through which cholesterol-lowering drugs can achieve plaque regression.</description><identifier>ISSN: 2731-0590</identifier><identifier>EISSN: 2731-0590</identifier><identifier>DOI: 10.1038/s44161-023-00412-w</identifier><identifier>PMID: 39196190</identifier><language>eng</language><publisher>England</publisher><subject>Animals ; Anticholesteremic Agents - pharmacology ; Anticholesteremic Agents - therapeutic use ; Aortic Diseases - metabolism ; Aortic Diseases - pathology ; Atherosclerosis - drug therapy ; Atherosclerosis - metabolism ; Atherosclerosis - pathology ; Cholesterol - blood ; Cholesterol - metabolism ; Chondrocytes - drug effects ; Chondrocytes - metabolism ; Chondrocytes - pathology ; Disease Models, Animal ; Male ; Mice ; Mice, Inbred C57BL ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - metabolism ; Muscle, Smooth, Vascular - pathology ; Myocytes, Smooth Muscle - drug effects ; Myocytes, Smooth Muscle - metabolism ; Myocytes, Smooth Muscle - pathology ; NF-kappa B - metabolism ; Plaque, Atherosclerotic - metabolism ; Plaque, Atherosclerotic - pathology ; Signal Transduction - drug effects ; Single-Cell Analysis</subject><ispartof>Nature Cardiovascular Research, 2024-02, Vol.3 (2), p.203-220</ispartof><rights>2024. 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Previous research showed that lowering ApoB-containing lipoproteins stops plaque inflammation, but how these drugs affect the heterogeneous population of plaque cells derived from smooth muscle cells (SMCs) is unknown. SMC-derived cells are the main cellular component of atherosclerotic lesions and the source of structural components that determine the size of plaques and their propensity to rupture and trigger thrombosis, the proximate cause of heart attack and stroke. Using lineage tracing and single-cell techniques to investigate the full SMC-derived cellular compartment in progressing and regressing plaques in mice, here we show that lowering ApoB-containing lipoproteins reduces nuclear factor kappa-light-chain-enhancer of activated B cells signaling in SMC-derived fibromyocytes and chondromyocytes and leads to depletion of these abundant cell types from plaques. 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| ispartof | Nature Cardiovascular Research, 2024-02, Vol.3 (2), p.203-220 |
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| subjects | Animals Anticholesteremic Agents - pharmacology Anticholesteremic Agents - therapeutic use Aortic Diseases - metabolism Aortic Diseases - pathology Atherosclerosis - drug therapy Atherosclerosis - metabolism Atherosclerosis - pathology Cholesterol - blood Cholesterol - metabolism Chondrocytes - drug effects Chondrocytes - metabolism Chondrocytes - pathology Disease Models, Animal Male Mice Mice, Inbred C57BL Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - metabolism Muscle, Smooth, Vascular - pathology Myocytes, Smooth Muscle - drug effects Myocytes, Smooth Muscle - metabolism Myocytes, Smooth Muscle - pathology NF-kappa B - metabolism Plaque, Atherosclerotic - metabolism Plaque, Atherosclerotic - pathology Signal Transduction - drug effects Single-Cell Analysis |
| title | Cholesterol lowering depletes atherosclerotic lesions of smooth muscle cell-derived fibromyocytes and chondromyocytes |
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