PMID- 35590466
OWN - NLM
STAT- MEDLINE
DCOM- 20220523
LR  - 20220716
IS  - 2058-7384 (Electronic)
IS  - 0394-6320 (Print)
IS  - 0394-6320 (Linking)
VI  - 36
DP  - 2022 Jan-Dec
TI  - COVID-19 and erythrocrine function: The roller coaster and danger.
PG  - 3946320221103151
LID - 10.1177/03946320221103151 [doi]
LID - 03946320221103151
AB  - Erythrocrine function refers to erythrocytes' ability to synthesize and release 
      active signaling molecules such as ATP and nitric oxide (NO). Erythrocyte NO 
      regulates its deformability and increases its perfusion and circulation that 
      prevent tissue hypoxia. Recently, there is a connotation between SARS-CoV-2 
      infection and erythrocrine function due to alteration in the release of NO and 
      ATP from erythrocytes. SARS-CoV-2 binds erythrocyte band3 protein, which has a 
      similar characteristic of ACE2, leading to alteration of erythrocyte physiology 
      like oxygen transport with development of hypoxia. Similarly, SARS-CoV-2 
      infection activates erythrocyte protein kinase C alpha (PKC-alpha), causing 
      significant changes in the erythrocyte functions. The erythrocytes can bind 
      SARS-CoV-2 and its active particles with subsequent virus delivery to the liver 
      and spleen macrophages. Thus, the erythrocytes act as elimination for SARS-CoV-2 
      in COVID-19. Moreover, the erythrocyte stored, release sphingosine-1 phosphate 
      (S1P) improves endothelial and regulates lymphocyte functions. SARS-CoV-2 ORF8 
      protein binds the porphyrin part of hemoglobin heme at the beta1 chain, causing 
      hemolysis and dysfunctional hemoglobin to reduce oxygen-carrying capacity. In 
      conclusion, SARS-CoV-2 infection and associated pro-inflammatory disorders lead 
      to abnormal erythrocrine function with subsequent inflammatory complications and 
      endothelial dysfunction due to deficiency of protective released molecules (NO, 
      G1P, and ATP) from functional erythrocytes. In vitro, preclinical, and clinical 
      studies are mandatory in this regard.
FAU - Al-Kuraishy, Hayder M
AU  - Al-Kuraishy HM
AD  - Department of Clinical Pharmacology and Medicine, College of Medicine, 
      AL-mustansiriyiah University, AL-mustansiriyiah, Iraq.
FAU - Al-Gareeb, Ali I
AU  - Al-Gareeb AI
AD  - Department of Clinical Pharmacology and Medicine, College of Medicine, 
      AL-mustansiriyiah University, AL-mustansiriyiah, Iraq.
FAU - Onohuean, Hope
AU  - Onohuean H
AUID- ORCID: 0000-0002-1890-6324
AD  - Biopharmaceutics Unit, Department of Pharmacology and Toxicology, School of 
      Pharmacy, 365672Kampala International University Uganda, Western Campus, 
      Ishaka-Bushenyi, Uganda.
FAU - El-Saber Batiha, Gaber
AU  - El-Saber Batiha G
AD  - Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, 
      Damanhour University, Damanhour, AlBeheira, Egypt.
LA  - eng
PT  - Journal Article
PL  - England
TA  - Int J Immunopathol Pharmacol
JT  - International journal of immunopathology and pharmacology
JID - 8911335
RN  - 0 (Hemoglobins)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Adenosine Triphosphate
MH  - *COVID-19
MH  - Hemoglobins
MH  - Humans
MH  - Hypoxia
MH  - Oxygen
MH  - SARS-CoV-2
PMC - PMC9124636
OTO - NOTNLM
OT  - COVID-19
OT  - Erythrocrine function
OT  - SARS-CoV-2
EDAT- 2022/05/21 06:00
MHDA- 2022/05/24 06:00
PMCR- 2022/05/19
CRDT- 2022/05/20 00:32
PHST- 2022/05/20 00:32 [entrez]
PHST- 2022/05/21 06:00 [pubmed]
PHST- 2022/05/24 06:00 [medline]
PHST- 2022/05/19 00:00 [pmc-release]
AID - 10.1177_03946320221103151 [pii]
AID - 10.1177/03946320221103151 [doi]
PST - ppublish
SO  - Int J Immunopathol Pharmacol. 2022 Jan-Dec;36:3946320221103151. doi: 
      10.1177/03946320221103151.