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Nano-medicine and Vascular Endothelial Dysfunction: Options and Delivery Strategies

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Abstract

The endothelium is a thin innermost layer of flat cells which release various mediators including endothelin-1 (ET-1), prostanoids, von Willebrand factor (vWF) and endothelium-derived relaxing factor (EDRF; nitric oxide) to regulate vascular tone. Endothelial nitric oxide synthase (eNOS) is a key enzyme that generates nitric oxide (NO). NO maintains vascular homeostasis and cardiac functions by influencing major vascular protective properties such as anti-platelet, anti-proliferative, anti-migratory, antioxidant and anti-inflammatory action in vessels. Abnormal endothelial production and release of NO lead to vascular endothelial dysfunction (VED) and further leads to pathogenesis in myocardial and other tissues. Numerous pharmacological agents such as angiotensin-converting enzyme inhibitors, statins, calcium channel blockers, ET-1 receptor antagonists, insulin sensitizers, antioxidants and supplements like tetrahydrobiopterin, arginine and folate have been implicated in the treatment of VED, but their therapeutic potency was restricted due to some unavoidable adverse effects. The new era with advances in nanotechnology and its ability to target a specific disease, nano-medicine explored an innovative gateway for advanced therapy for VED. The present commentary reveals the various available, pipeline nano-medicine, their interaction with endothelium and in other associated pathological conditions and their delivery strategies for target-specific treatment of VED.

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Abbreviations

ACE-1:

Angiotensin-converting enzyme 1

ADMA:

Asymmetric dimethylarginine

AGE:

Advanced glycation end product

Akt:

Protein kinase B

BH4:

Tetrahydrobiopterin

CAD:

Coronary artery disease

CDK:

Cyclin-dependent kinase

CETP:

Cholesteryl ester transfer protein

CVD:

Cardiovascular disease

CXCL12:

C-X-C motif chemokine 12

DAMPs:

Endogenous damage-associated molecular patterns

EAhy926 cells:

Endothelial-like cells

ECs:

Endothelial cells

EDRF:

Endothelium-derived relaxing factor

eNOS:

Endothelial nitric oxide synthase

ET-1:

Endothelin-1

FAD:

Flavin adenine dinucleotide

FMN:

Flavin mononucleotide

GGTase-I:

Geranylgeranyltransferase-1

GLP-1:

Glucagon-like peptide 1

Hif-1α:

Hypoxia-inducible factor-1α

HMG-CoA:

3-Hydroxy 3-methylglutaryl coenzyme A

HO-1:

Heme oxygenase-1

HUVECs:

Human umbilical vein endothelial cells

ICAM-1:

Intercellular adhesion molecule 1

IGF-1R:

Insulin-like growth factor 1 receptor

IL-6:

Interleukin-6

JAK:

Janus kinase

LOX-1:

Lectin-like oxidized low-density lipoprotein receptor-1

LPS:

Lipopolysaccharide

MCP-1:

Monocyte chemoattractant protein

MNBs:

Magnetic nano-beads

MRI:

Magnetic resonance imaging

mTOR:

Mammalian target of rapamycin

NADPH:

Nicotinamide adenine dinucleotide phosphate

NFk-β:

Nuclear factor kappa-β

NO:

Nitric oxide

NPs:

Nanoparticles

PAK1:

p21 protein (Cdc42/Rac)-activated kinase 1

PAMPs:

Pathogen-associated molecular patterns

PECAM:

Platelet-endothelial cell adhesion molecule-1

PET–MRI:

Positron emission tomography–magnetic resonance imaging

PIK3R2:

Phosphatidylinositol 3-kinase regulatory subunit beta receptor

PI3K:

Phosphatidylinositol-3-kinases

PKA:

Protein kinase A

PLGA-PEG:

Poly(lactide-co-glycolide)–poly(ethylene glycol) polymer

PPAR:

Peroxisome proliferator-activated receptor

PRRs:

Pattern recognition receptors

PTPase:

Protein tyrosine phosphatase

ROS:

Reactive oxygen species

SPIONs:

Superparamagnetic iron oxide NPs

SPRED-I:

Sprouty-related protein I

S1P:

Sphingosine-1-phosphate

TLRs:

Toll-like receptors

TNF-α:

Tumor necrosis factor-α

USIOPs:

Ultra-small superparamagnetic iron oxide particles

VCAM-1:

Vascular cell adhesion molecule 1

VED:

Vascular endothelial dysfunction

VEGF-A:

Vascular endothelial growth factor-A

VSMCs:

Vascular smooth muscle cells

vWF:

Von Willebrand factor

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Acknowledgements

The authors are grateful to the authority of the Amity Institute of Pharmacy, Amity University, Gurugram, Haryana, India, for providing the necessary facilities.

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Authors and Affiliations

  1. Fortis Healthcare Ltd, Gurugram, India

    Gaurav Taneja, Akash Sud, Narayan Pendse & Bishnu Panigrahi

  2. Department of Pharmaceutical Science, Amity Institute of Pharmacy, Amity University, Noida, UP, India

    Ashish Kumar

  3. Cardiovascular Division, Department of Pharmacology, Amity Institute of Pharmacy, Amity University, Gurugram, Haryana, 122051, India

    Arun K. Sharma

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  1. Gaurav Taneja
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Taneja, G., Sud, A., Pendse, N. et al. Nano-medicine and Vascular Endothelial Dysfunction: Options and Delivery Strategies. Cardiovasc Toxicol 19, 1–12 (2019). https://doi.org/10.1007/s12012-018-9491-x

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