The Role of ACE2 Receptor and Its Polymorphisms in COVID-19 Infection and Severity and Its Association with Lipid Profile, Thrombin, and D-Dimer Levels in Iraqi Patients: A Cross-Sectional Study

被引:0
|
作者
Hatem, Ban Adnan [1 ]
Jabir, Ferdous A. [2 ]
机构
[1] Al Qadisiyah Univ, Coll Sci, Chem Dept, Al Diwaniyah, Iraq
[2] Al Qadisiyah Univ, Coll Med, Biochem Dept, Al Diwaniyah, Iraq
关键词
ACE2; polymorphism; COVID-19; D-dimer; Lipid profile; Severity; Thrombin; PREDICTION; DIAGNOSIS; VIRUS;
D O I
10.1007/s10528-024-10890-7
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
COVID-19 patients experience a complex interplay involving ACE2, thrombin, D-dimer, and lipid profile, yet its full understanding remains elusive. ACE2, a pivotal regulator of the renin-angiotensin system and the primary receptor for SARS-CoV-2 undergoes downregulation upon viral binding, potentially leading to severe cases with acute respiratory distress syndrome (ARDS). A specific ACE2 gene polymorphism (rs2285666) may be associated with COVID-19 susceptibility, with the A allele potentially increasing infection risk. COVID-19 disease progression is linked to coagulation abnormalities, but the exact connection with thrombin and D-dimer remains uncertain. A study examining coagulation parameters in COVID-19 patients admitted to Al-Diwania Educational Hospital from February to May 2022 found that thrombin and D-dimer levels were directly related to disease severity. Severe cases exhibited significantly altered coagulation function compared to mild and recovered cases, with notably higher D-dimer levels and elevated thrombin serum concentrations. Moreover, dyslipidemia, particularly low HDL cholesterol, is a prevalent comorbidity in COVID-19 patients and may be linked to worse outcomes. In conclusion, COVID-19 is associated with a prothrombotic state and dysregulation of the renin-angiotensin system due to ACE2 downregulation following viral binding. The intricate interplay between ACE2, thrombin, D-dimer, and lipid profile necessitates further investigation. The multifaceted nature of the disease demands continued research to unravel its pathogenesis and identify potential therapeutic targets.
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