Nesfatin-1 functions as a switch for phenotype transformation and proliferation of VSMCs in hypertensive vascular remodeling.
@article{Lu2018Nesfatin1FA, title={Nesfatin-1 functions as a switch for phenotype transformation and proliferation of VSMCs in hypertensive vascular remodeling.}, author={Qing-Bo Lu and Huiping Wang and Zihan Tang and Han Cheng and Qiong Du and Yuan-Ben Wang and Wu-Bing Feng and Ke-Xue Li and Weiwei Cai and Liying Qiu and Hai-Jian Sun}, journal={Biochimica et biophysica acta. Molecular basis of disease}, year={2018}, volume={1864 6 Pt A}, pages={ 2154-2168 } }
40 Citations
LncRNA MRAK048635_P1 is critical for vascular smooth muscle cell function and phenotypic switching in essential hypertension
- Biology, MedicineBioscience reports
- 2019
It is revealed that decreased MRAK048635_P1 is probably an important factor for vascular remodeling by affecting VSMC cell function and phenotypic switching in essential hypertension.
p22phox promotes Ang-II-induced vascular smooth muscle cell phenotypic switch by regulating KLF4 expression.
- Biology, ChemistryBiochemical and biophysical research communications
- 2019
Magnolol alleviates hypoxia-induced pulmonary vascular remodeling through inhibition of phenotypic transformation in pulmonary arterial smooth muscle cells.
- BiologyBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
- 2022
Role of the signal transducer and activator of transcription 3 protein in the proliferation of vascular smooth muscle cells
- BiologyVascular
- 2020
Studying the mechanism of VSMC proliferation induced by the STAT3 pathway is valuable for finding therapeutic targets for CVD.
Nesfatin-1 suppresses peripheral arterial remodeling without elevating blood pressure in mice
- BiologyEndocrine connections
- 2019
Evaluating the vasoprotective and vasopressor effects of nesfatin-1 at different doses in mouse models demonstrated that nesFatin- 1 can be a therapeutic target for improved treatment of peripheral artery disease.
Imperatorin alleviates the abnormal proliferation, migration, and foaming of ox-LDL-induced VSMCs through regulating PI3K/Akt/mTOR signaling pathway
- Biology, Chemistry
- 2020
lncRNA 430945 promotes the proliferation and migration of vascular smooth muscle cells via the ROR2/RhoA signaling pathway in atherosclerosis
- BiologyMolecular medicine reports
- 2019
It was found that the expression of lncRNA 430945 was high in human AS tissues, which in turn promoted angiotensin II (AngII)-induced VSMC proliferation and migration and activated the signaling pathways associated with ROR2 and Ras homolog gene family member A (RhoA).
Urantide alleviates the symptoms of atherosclerotic rats in vivo and in vitro models through the JAK2/STAT3 signaling pathway.
- BiologyEuropean journal of pharmacology
- 2021
Extracellular Vesicle-Mediated Vascular Cell Communications in Hypertension: Mechanism Insights and Therapeutic Potential of ncRNAs
- Biology, MedicineCardiovascular Drugs and Therapy
- 2020
The current findings focusing on the emerging roles of extracellular vesicle-carrying ncRNAs in the pathologies of hypertension and its associated vascular remodeling are discussed and highlighted.
Expression of Long Noncoding RNA LIPCAR Promotes Cell Proliferation, Cell Migration, and Change in Phenotype of Vascular Smooth Muscle Cells
- BiologyMedical science monitor : international medical journal of experimental and clinical research
- 2019
The data suggest that overexpression of LIPCAR promotes cell proliferation, migration, and phenotypic switch of vascular smooth muscle cells.
References
SHOWING 1-10 OF 68 REFERENCES
NLRP3 Gene Deletion Attenuates Angiotensin II-Induced Phenotypic Transformation of Vascular Smooth Muscle Cells and Vascular Remodeling
- Biology, MedicineCellular Physiology and Biochemistry
- 2017
NLRP3 inflammasome activation contributes to Ang II-induced VSMC phenotypic transformation and proliferation as well as vascular remodeling and hypertension.
Chicoric acid prevents PDGF-BB-induced VSMC dedifferentiation, proliferation and migration by suppressing ROS/NFκB/mTOR/P70S6K signaling cascade
- BiologyRedox biology
- 2018
Vascular smooth muscle cell in atherosclerosis
- BiologyActa physiologica
- 2015
Proinflammatory signals play a crucial role in further dedifferentiation of VSMCs in affected vessels and propagation of pathological vascular remodelling in chronic inflammation.
NLRP3 inflammasome activation contributes to VSMC phenotypic transformation and proliferation in hypertension
- Biology, ChemistryCell Death and Disease
- 2017
Results indicate that NLRP3 inflammasome activation response to histone acetylation and NFκB activation contributes to VSMC phenotype switching and proliferation and vascular remodeling in hypertension.
Salusin-β contributes to vascular remodeling associated with hypertension via promoting vascular smooth muscle cell proliferation and vascular fibrosis.
- Biology, MedicineBiochimica et biophysica acta
- 2015
Vascular Smooth Muscle Cells in Atherosclerosis.
- BiologyCirculation research
- 2016
There is now compelling evidence that a full understanding of VSMC behavior in Atherosclerosis is critical to identify therapeutic targets to both prevent and treat atherosclerosis.
The vascular smooth muscle cell in arterial pathology: a cell that can take on multiple roles.
- BiologyCardiovascular research
- 2012
The medial VSMC is the organizer of the inwardly directed angiogenic response arising from the adventitia by overexpressing vascular endothelial growth factor in response to lipid-stimulated peroxisome proliferator-activated receptor-γ, and probably also the organizers of the adventitial immune response by secreting chemokines.
Signaling Pathways Regulating Vascular Smooth Muscle Cell Differentiation
- Biology, MedicineVascular
- 2009
The focus of this review is to provide an overview of the current state of knowledge of molecular mechanisms involved in controlling phenotypic switching of VSMCs, with particular focus on examination of the signaling pathways that regulate this process.
STAT3 Protein Regulates Vascular Smooth Muscle Cell Phenotypic Switch by Interaction with Myocardin*
- Biology, MedicineThe Journal of Biological Chemistry
- 2015
The results of this study indicate that the JAK-STAT3 signaling pathway plays a key role in controlling the phenotypic switch of VSMCs through the interactions between STAT3 and myocardin by various coordinated gene regulation pathways and feedback loops.
A novel adipocytokine, nesfatin-1 modulates peripheral arterial contractility and blood pressure in rats.
- BiologyBiochemical and biophysical research communications
- 2012