Prokineticin signaling in heart-brain developmental axis: Therapeutic options for heart and brain injuries

Pharmacol Res. 2020 Oct:160:105190. doi: 10.1016/j.phrs.2020.105190. Epub 2020 Sep 13.

Abstract

Heart and brain development occur simultaneously during the embryogenesis, and both organ development and injuries are interconnected. Early neuronal and cardiac injuries share mutual cellular events, such as angiogenesis and plasticity that could either delay disease progression or, in the long run, result in detrimental health effects. For this reason, the common mechanisms provide a new and previously undervalued window of opportunity for intervention. Because angiogenesis, cardiogenesis and neurogenesis are essential for the development and regeneration of the heart and brain, we discuss therein the role of prokineticin as an angiogenic neuropeptide in heart-brain development and injuries. We focus on the role of prokineticin signaling and the effect of drugs targeting prokineticin receptors in neuroprotection and cardioprotection, with a special emphasis on heart failure, neurodegenerativParkinson's disease and ischemic heart and brain injuries. Indeed, prokineticin triggers common pro-survival signaling pathway in heart and brain. Our review aims at stimulating researchers and clinicians in neurocardiology to focus on the role of prokineticin signaling in the reciprocal interaction between heart and brain. We hope to facilitate the discovery of new treatment strategies, acting in both heart and brain degenerative diseases.

Keywords: Angiogenesis; Brain; GPCR; Heart; Heart failure; Neuropeptide; Parkinson; Prokineticin; Regeneration.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Brain / growth & development*
  • Brain / physiology
  • Brain Diseases / genetics*
  • Heart / growth & development*
  • Heart / physiology
  • Heart Diseases / genetics*
  • Humans
  • Neurogenesis / genetics
  • Receptors, G-Protein-Coupled / drug effects
  • Receptors, G-Protein-Coupled / genetics
  • Receptors, G-Protein-Coupled / physiology
  • Vascular Endothelial Growth Factor, Endocrine-Gland-Derived / genetics*
  • Vascular Endothelial Growth Factor, Endocrine-Gland-Derived / physiology*

Substances

  • PROKR1 protein, human
  • Receptors, G-Protein-Coupled
  • Vascular Endothelial Growth Factor, Endocrine-Gland-Derived