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Cardiovascular Toxicology

, Volume 19, Issue 1, pp 1–12 | Cite as

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

  • Gaurav Taneja
  • Akash Sud
  • Narayan Pendse
  • Bishnu Panigrahi
  • Ashish Kumar
  • Arun K. SharmaEmail author
Article

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.

Keywords

Vascular endothelial dysfunction Nano-medicine Nanoparticle eNOS Cardiovascular disorders 

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

Notes

Acknowledgements

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

Compliance with Ethical Standards

Conflict of interest

No conflict of interest is declared.

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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2018

Authors and Affiliations

  • Gaurav Taneja
    • 1
  • Akash Sud
    • 1
  • Narayan Pendse
    • 1
  • Bishnu Panigrahi
    • 1
  • Ashish Kumar
    • 2
  • Arun K. Sharma
    • 3
    Email author
  1. 1.Fortis Healthcare LtdGurugramIndia
  2. 2.Department of Pharmaceutical Science, Amity Institute of PharmacyAmity UniversityNoidaIndia
  3. 3.Cardiovascular Division, Department of Pharmacology, Amity Institute of PharmacyAmity UniversityGurugramIndia

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