Vascular Smooth Muscle Cells: A Therapeutic Target in Atherosclerosis
Background: Vascular smooth muscle cells (VSMCs) are involved in atherosclerotic plaque development. The formation of VSMC-originated foam cells, phenotypic switching, and VSMC proliferation, migration, apoptosis, and autophagy play different roles in atherosclerosis (AS)....
Saved in:
| Main Authors: | , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
IMR Press
2025-06-01
|
| Series: | Reviews in Cardiovascular Medicine |
| Subjects: | |
| Online Access: | https://www.imrpress.com/journal/RCM/26/6/10.31083/RCM28240 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1850089029414944768 |
|---|---|
| author | Lingna Zhao Li Zhao Deshen Liu Fangze Huang Qinbao Peng Jun Lu Jiaguo Zhou Shaoyi Zheng Xiu Liu |
| author_facet | Lingna Zhao Li Zhao Deshen Liu Fangze Huang Qinbao Peng Jun Lu Jiaguo Zhou Shaoyi Zheng Xiu Liu |
| author_sort | Lingna Zhao |
| collection | DOAJ |
| description | Background: Vascular smooth muscle cells (VSMCs) are involved in atherosclerotic plaque development. The formation of VSMC-originated foam cells, phenotypic switching, and VSMC proliferation, migration, apoptosis, and autophagy play different roles in atherosclerosis (AS). Main Body: Foam cell formation promotes the generation and evolution of atherosclerotic plaques. The VSMC phenotype, switching from contractile to other forms, is important in the formation and progression of AS. VSMC proliferation, migration, and apoptosis affect the stability of atherosclerotic plaques through the fibrous cap. VSMC proliferation and migration can increase the thickness of the fibrous cap of the plaques, which protects plaques from rupture and is beneficial for slowing the occurrence of advanced lesions. However, apoptosis can accelerate plaque rupturing and trigger severe cardiovascular disease. The autophagy of VSMCs has a protective influence on safeguarding cellular homeostasis in the early stages of AS. However, increased autophagy of VSMCs in the late stages of AS can lead to cell death, thereby affecting the stability of late-stage plaques. This review comprehensively reviews recent research on genetic proteins and mechanisms influencing various aspects of VSMCs, including VSMC-derived foam cells, phenotypic switching, proliferation, migration, apoptosis, and autophagy. Additionally, this review aimed to examine the implications of VSMCs for AS and discussed several regulators that can impact the progression of this condition. Our review thoroughly summarizes the latest research developments in this field. Conclusion: Based on the vital role of VSMCs in AS, this review provides an overview of the latest factors and mechanisms based on VSMC-derived foam cells, phenotype switching, proliferation, migration, apoptosis, and autophagy. The review also introduces certain regulators that can inhibit the development of AS. An understanding of the role of VSMCs aids in identifying new targets and directions for advancing innovative anti-atherosclerotic therapeutic regimens and provides new insights into the development of treatments for AS. |
| format | Article |
| id | doaj-art-99fc8d2bdd7c4effa69fbeb8ae901599 |
| institution | DOAJ |
| issn | 1530-6550 |
| language | English |
| publishDate | 2025-06-01 |
| publisher | IMR Press |
| record_format | Article |
| series | Reviews in Cardiovascular Medicine |
| spelling | doaj-art-99fc8d2bdd7c4effa69fbeb8ae9015992025-08-20T02:42:53ZengIMR PressReviews in Cardiovascular Medicine1530-65502025-06-012662824010.31083/RCM28240S1530-6550(25)01795-8Vascular Smooth Muscle Cells: A Therapeutic Target in AtherosclerosisLingna Zhao0Li Zhao1Deshen Liu2Fangze Huang3Qinbao Peng4Jun Lu5Jiaguo Zhou6Shaoyi Zheng7Xiu Liu8Department of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, Guangdong, ChinaDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, Guangdong, ChinaDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, Guangdong, ChinaDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, Guangdong, ChinaDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, Guangdong, ChinaDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, Guangdong, ChinaDepartment of Pharmacology, Cardiac and Cerebral Vascular Research Center, Zhongshan School of Medicine, Sun Yat-sen University, 510080 Guangzhou, Guangdong, ChinaDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, Guangdong, ChinaDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, 510515 Guangzhou, Guangdong, ChinaBackground: Vascular smooth muscle cells (VSMCs) are involved in atherosclerotic plaque development. The formation of VSMC-originated foam cells, phenotypic switching, and VSMC proliferation, migration, apoptosis, and autophagy play different roles in atherosclerosis (AS). Main Body: Foam cell formation promotes the generation and evolution of atherosclerotic plaques. The VSMC phenotype, switching from contractile to other forms, is important in the formation and progression of AS. VSMC proliferation, migration, and apoptosis affect the stability of atherosclerotic plaques through the fibrous cap. VSMC proliferation and migration can increase the thickness of the fibrous cap of the plaques, which protects plaques from rupture and is beneficial for slowing the occurrence of advanced lesions. However, apoptosis can accelerate plaque rupturing and trigger severe cardiovascular disease. The autophagy of VSMCs has a protective influence on safeguarding cellular homeostasis in the early stages of AS. However, increased autophagy of VSMCs in the late stages of AS can lead to cell death, thereby affecting the stability of late-stage plaques. This review comprehensively reviews recent research on genetic proteins and mechanisms influencing various aspects of VSMCs, including VSMC-derived foam cells, phenotypic switching, proliferation, migration, apoptosis, and autophagy. Additionally, this review aimed to examine the implications of VSMCs for AS and discussed several regulators that can impact the progression of this condition. Our review thoroughly summarizes the latest research developments in this field. Conclusion: Based on the vital role of VSMCs in AS, this review provides an overview of the latest factors and mechanisms based on VSMC-derived foam cells, phenotype switching, proliferation, migration, apoptosis, and autophagy. The review also introduces certain regulators that can inhibit the development of AS. An understanding of the role of VSMCs aids in identifying new targets and directions for advancing innovative anti-atherosclerotic therapeutic regimens and provides new insights into the development of treatments for AS.https://www.imrpress.com/journal/RCM/26/6/10.31083/RCM28240atherosclerosisvascular smooth muscle cellvascular smooth muscle cell-derived foam cellphenotypic switchingapoptosisautophagy |
| spellingShingle | Lingna Zhao Li Zhao Deshen Liu Fangze Huang Qinbao Peng Jun Lu Jiaguo Zhou Shaoyi Zheng Xiu Liu Vascular Smooth Muscle Cells: A Therapeutic Target in Atherosclerosis Reviews in Cardiovascular Medicine atherosclerosis vascular smooth muscle cell vascular smooth muscle cell-derived foam cell phenotypic switching apoptosis autophagy |
| title | Vascular Smooth Muscle Cells: A Therapeutic Target in Atherosclerosis |
| title_full | Vascular Smooth Muscle Cells: A Therapeutic Target in Atherosclerosis |
| title_fullStr | Vascular Smooth Muscle Cells: A Therapeutic Target in Atherosclerosis |
| title_full_unstemmed | Vascular Smooth Muscle Cells: A Therapeutic Target in Atherosclerosis |
| title_short | Vascular Smooth Muscle Cells: A Therapeutic Target in Atherosclerosis |
| title_sort | vascular smooth muscle cells a therapeutic target in atherosclerosis |
| topic | atherosclerosis vascular smooth muscle cell vascular smooth muscle cell-derived foam cell phenotypic switching apoptosis autophagy |
| url | https://www.imrpress.com/journal/RCM/26/6/10.31083/RCM28240 |
| work_keys_str_mv | AT lingnazhao vascularsmoothmusclecellsatherapeutictargetinatherosclerosis AT lizhao vascularsmoothmusclecellsatherapeutictargetinatherosclerosis AT deshenliu vascularsmoothmusclecellsatherapeutictargetinatherosclerosis AT fangzehuang vascularsmoothmusclecellsatherapeutictargetinatherosclerosis AT qinbaopeng vascularsmoothmusclecellsatherapeutictargetinatherosclerosis AT junlu vascularsmoothmusclecellsatherapeutictargetinatherosclerosis AT jiaguozhou vascularsmoothmusclecellsatherapeutictargetinatherosclerosis AT shaoyizheng vascularsmoothmusclecellsatherapeutictargetinatherosclerosis AT xiuliu vascularsmoothmusclecellsatherapeutictargetinatherosclerosis |