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β-Adrenergic receptor, an essential target in cardiovascular diseases

  • Daniel Chikere Ali
  • Muhammad Naveed
  • Andrew Gordon
  • Fatima Majeed
  • Muhammad Saeed
  • Michael I. Ogbuke
  • Muhammad Atif
  • Hafiz Muhammad Zubair
  • Li ChangxingEmail author
Article

Abstract

β-Adrenergic receptors (βARs) belong to a large family of cell surface receptors known as G protein–coupled receptors (GPCRs). They are coupled to Gs protein (Gαs) for the activation of adenylyl cyclase (AC) yielding cyclic AMP (CAMP), and this provides valuable responses, which can affect the cardiac function such as injury. The binding of an agonist to βAR enhances conformation changes that lead to the Gαs subtype of heterotrimeric G protein which is the AC stimulatory G protein for activation of CAMP in the cells. However, cardiovascular diseases (CVD) have been reported as having an increased rate of death and β1AR, and β2AR are a promising tool that improves the regulatory function in the cardiovascular system (CVS) via signaling. It increases the Gα level, which activates βAR kinase (βARK) that affects and enhances the progression of heart failure (HF) through the activation of cardiomyocyte βARs. We also explained that an increase in GPCR kinases (GRKs) would practically improve the HF pathogenesis and this occurs via the desensitization of βARs, which causes the loss of contractile reserve. The consistency or overstimulation of catecholamines contributes to CVD such as stroke, HF, and cardiac hypertrophy. When there is a decrease in catecholamine responsiveness, it causes aging in old people because the reduction of βAR sensitivity and density in the myocardium enhances downregulation of βARs to AC in the human heart.

Keywords

Cardiovascular disease Heart failure β-Adrenergic receptor Catecholamines Adenylyl cyclase GPCR 

Notes

Acknowledgments

We are very grateful to Ali Ozoemena for his unalloyed pieces of advice to complete this article. We are thankful to Chinese Scholarship Council (CSC) for funding our research scholar FATIMA Majeed in her doctorate studies. Furthermore, all the authors of the manuscript also thank and acknowledge their respective Universities and Institutes.

Funding information

The Qinghai Science and Technology Department Project (Nos. 2018-ZJ-730 & 2019-SF-134) supported this work.

Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.

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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  • Daniel Chikere Ali
    • 1
  • Muhammad Naveed
    • 2
  • Andrew Gordon
    • 3
  • Fatima Majeed
    • 4
  • Muhammad Saeed
    • 5
  • Michael I. Ogbuke
    • 6
  • Muhammad Atif
    • 7
  • Hafiz Muhammad Zubair
    • 8
  • Li Changxing
    • 9
    Email author
  1. 1.Department of Microbiological and Biochemical Pharmacy, School of Life ScienceChina Pharmaceutical UniversityNanjingPeople’s Republic of China
  2. 2.Department of Clinical Pharmacology, School of PharmacyNanjing Medical UniversityNanjingPeople’s Republic of China
  3. 3.Department of Pharmacognosy, School of PharmacyChina Pharmaceutical UniversityNanjingPeople’s Republic of China
  4. 4.Department of Nutrition and Food Hygiene, School of Public HealthNanjing Medical UniversityNanjingPeople’s Republic of China
  5. 5.Faculty of Animal Production and TechnologyThe Cholistan University of Veterinary and Animal SciencesPunjab ProvincePakistan
  6. 6.Department of Pharmacy, School of Pharmacy, China Pharmaceutical UniversityNanjingPeople’s Republic of China
  7. 7.Faculty of Pharmacy and Alternative MedicineThe Islamia University of BahawalpurBahawalpurPakistan
  8. 8.Department of Pharmacology, School of Basic Medical SciencesNanjing Medical UniversityNanjingPeople’s Republic of China
  9. 9.Department of Human AnatomyMedical College of Qinghai UniversityXiningPeople’s Republic of China

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