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Neurosci Lett. 2019 Sep 7;712:134471. doi: 10.1016/j.neulet.2019.134471. [Epub ahead of print]

Updated mechanisms underlying sickle cell disease-associated pain.

Author information

1
Department of Anesthesiology, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ 07103, USA.
2
Rutgers Graduate School of Biomedical Sciences, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ 07103, USA.
3
Department of Anesthesiology, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ 07103, USA; Rutgers Graduate School of Biomedical Sciences, New Jersey Medical School, Rutgers, The State University of New Jersey, Newark, NJ 07103, USA. Electronic address: yuanxiang.tao@njms.rutgers.edu.

Abstract

Sickle cell disease (SCD) is one of the most common severe genetic diseases around the world. A majority of SCD patients experience intense pain, leading to hospitalization, and poor quality of life. Opioids form the bedrock of pain management, but their long-term use is associated with severe side effects including hyperalgesia, tolerance and addiction. Recently, excellent research has shown some new potential mechanisms that underlie SCD-associated pain. This review focused on how transient receptor potential vanilloid 1, endothelin-1/endothelin type A receptor, and cannabinoid receptors contributed to the pathophysiology of SCD-associated pain. Understanding these mechanisms may open a new avenue in managing SCD-associated pain and improving quality of life for SCD patients.

KEYWORDS:

Cannabinoid receptors; Endothelin type A receptor; Endothelin-1; Pain; Sickle cell disease; TRPV1

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