Mathematical model of hypertension-induced arterial remodeling: A chemo-mechanical approach

Wilstein, Zahava; Alligood, Daniel M.; McLure, Valerie L.; Miller, Austinn C.

doi:10.1016/j.mbs.2018.05.002

Cited by 8 publications

(8 citation statements)

References 66 publications

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“…Their findings demonstrate that tissue blood flow recovery was impaired in eNOS-knockout mice due to the inability to sufficiently vasodilate collaterals and not because of impaired arteriogenesis [102]. These findings were supported by several studies using mathematical modeling that showed that collateral vasodilation is a critical triggering factor for significant blood flow compensation to occur following arterial occlusion [103,104].…”

Section: The Effect Of Hemodynamics On Smooth Muscle Cell Phenotype During Arteriogenesismentioning

confidence: 77%

Role of Vascular Smooth Muscle Cell Phenotype Switching in Arteriogenesis

Ashraf

Zen

2021

IJMS

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Arteriogenesis is one of the primary physiological means by which the circulatory collateral system restores blood flow after significant arterial occlusion in peripheral arterial disease patients. Vascular smooth muscle cells (VSMCs) are the predominant cell type in collateral arteries and respond to altered blood flow and inflammatory conditions after an arterial occlusion by switching their phenotype between quiescent contractile and proliferative synthetic states. Maintaining the contractile state of VSMC is required for collateral vascular function to regulate blood vessel tone and blood flow during arteriogenesis, whereas synthetic SMCs are crucial in the growth and remodeling of the collateral media layer to establish more stable conduit arteries. Timely VSMC phenotype switching requires a set of coordinated actions of molecular and cellular mediators to result in an expansive remodeling of collaterals that restores the blood flow effectively into downstream ischemic tissues. This review overviews the role of VSMC phenotypic switching in the physiological arteriogenesis process and how the VSMC phenotype is affected by the primary triggers of arteriogenesis such as blood flow hemodynamic forces and inflammation. Better understanding the role of VSMC phenotype switching during arteriogenesis can identify novel therapeutic strategies to enhance revascularization in peripheral arterial disease.

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Section: The Effect Of Hemodynamics On Smooth Muscle Cell Phenotype During Arteriogenesismentioning

confidence: 77%

Role of Vascular Smooth Muscle Cell Phenotype Switching in Arteriogenesis

Ashraf

Zen

2021

IJMS

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“…Vascular remodeling is a characteristic pathological feature of hypertension [19]. The main mechanism of vascular remodeling is the activation of silent VSMCs in a physiological state, which leads to abnormal VSMC proliferation and the formation of neointima [20].…”

Section: Discussionmentioning

confidence: 99%

LncRNA MRAK048635_P1 is critical for vascular smooth muscle cell function and phenotypic switching in essential hypertension

et al. 2019

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Vascular remodeling caused by essential hypertension is a leading cause of death in patients, and vascular smooth muscle cell (VSMC) dysfunction and phenotypic switching result in vascular remodeling. Therefore, inhibiting cell dysfunction and phenotypic switching in VSMCs may be a new treatment strategy for essential hypertension. The aim of the current study is to explore the roles of long non-coding RNA (lncRNA) MRAK048635_P1 in VSMC function and phenotypic switching. The MRAK048635_P1 level was determined in spontaneously hypertensive rats (SHRs) and VSMCs isolated from SHRs. MRAK048635_P1 was knocked down using a specific siRNA in VSMCs isolated from the thoracic aorta of SHRs and Wistar–Kyoto rats. Then, the proliferation and migration of VSMCs were determined using a cell counting kit-8 (CCK-8), a 3H labeling method, a transwell assay, and a wound healing assay. Flow cytometry was used to test the effect of MRAK048635_P1 on VSMC apoptosis. The protein and mRNA levels of associated genes were measured through Western blotting, immunofluorescence, and Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). MRAK048635_P1 showed low expression during hypertension in vivo and in vitro. Down-regulation of lncRNA MRAK048635_P1 promoted proliferation and migration and inhibited apoptosis in VSMCs isolated from healthy rat vascular tissue and SHR-derived VSMCs. Importantly, we also found that down-regulation of MRAK048635_P1 could induce VSMC phenotypic switching from a contractile to a secretory phenotype. In conclusion, our findings reveal that decreased MRAK048635_P1 is probably an important factor for vascular remodeling by affecting VSMC cell function and phenotypic switching in essential hypertension.

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“…Test-cases was used to investigate the evolution of the lesion in pro-atherogenic flow regions. Ordinary differential equations (ODEs) and delay differential equations (DDEs) of kinetic equations type have been used to develop models of tissue growth time evolution for atherosclerosis (Bulelzai and Dubbeldam, 2012), hypertension (Wilstein et al, 2018), intimal hyperplasia (Schwartz et al, 1996;Donadoni et al, 2017), tissue-engineered vascular grafts (Khosravi et al, 2020) and wound healing inflammation (Nagaraja et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Multiscale bio-chemo-mechanical model of intimal hyperplasia

Jansen

Escriva

Godeferd

et al. 2022

Biomech Model Mechanobiol

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We consider a computational multiscale framework of a bio-chemo-mechanical model for intimal hyperplasia. With respect to existing models, we investigate the interactions between hemodynamics, cellular dynamics and biochemistry on the development of the pathology. Within the arterial wall, we propose a mathematical model consisting of kinetic differential equations for key vascular cell types, collagen and growth factors. The luminal hemodynamics is modelled with the Navier-Stokes equations. Coupling hypothesis among time and space scales are proposed to build a tractable modelling of such a complex multifactorial and multiscale pathology. A one-dimensional numerical test-case is presented for validation by comparing the results of the framework with experiments at short and long timescales. Our model permits to capture many cellular phenomena which have a central role in the physiopathology of intimal hyperplasia. Results are quantitatively and qualitatively consistent with experimental findings at both short and long timescales.

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Mathematical model of hypertension-induced arterial remodeling: A chemo-mechanical approach

Cited by 8 publications

References 66 publications

Role of Vascular Smooth Muscle Cell Phenotype Switching in Arteriogenesis

Role of Vascular Smooth Muscle Cell Phenotype Switching in Arteriogenesis

LncRNA MRAK048635_P1 is critical for vascular smooth muscle cell function and phenotypic switching in essential hypertension

Multiscale bio-chemo-mechanical model of intimal hyperplasia

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