An Integrated Approach of the Potential Underlying Molecular Mechanistic Paradigms of SARS-CoV-2-Mediated

Anmol Goyal1, Rajendra Prasad2, Parul Goel2

  • 1Department of Community Medicine, Gian Sagar Medical College and Hospital, Ram Nagar, Rajpura, Patiala, Punjab India.

Insights

This review explores how apoptosis, inflammation, hypoxia, and angiogenesis signaling pathways may cause thrombosis in COVID-19. Understanding these mechanisms could reveal new therapeutic targets for treating COVID-19 related blood clots.

Area of Science:

  • * Molecular Biology
  • * Pathology
  • * Virology

Background:

  • * Coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, is a global pandemic with no specific treatments.
  • * COVID-19 is increasingly linked to thrombosis and coagulopathy.
  • * The molecular mechanisms underlying COVID-19-associated thrombosis are not fully understood.

Purpose of the Study:

  • * To review the hypothetical crosstalk between distinct signaling pathways contributing to thrombotic events in COVID-19.
  • * To explore potential molecular mechanisms driving thrombosis in SARS-CoV-2 infection.
  • * To identify promising therapeutic targets for COVID-19.

Main Methods:

  • * Literature review of existing studies on COVID-19, thrombosis, and related signaling pathways.
  • * Analysis of hypothetical interactions between apoptosis, inflammation, hypoxia, and angiogenesis.
  • * Synthesis of current knowledge to propose mechanistic links to thrombotic events.

Main Results:

  • * Hypothesized crosstalk between apoptosis, inflammation, hypoxia, and angiogenesis pathways in SARS-CoV-2 infection.
  • * These pathways may collectively contribute to the activation of the coagulation cascade.
  • * Potential molecular mechanisms for COVID-19-associated thrombosis are elucidated.

Conclusions:

  • * Understanding the interplay of these signaling pathways is crucial for unraveling COVID-19 pathogenesis.
  • * The identified pathways represent potential targets for novel therapeutic interventions.
  • * Further research is warranted to validate these hypothetical mechanisms and therapeutic strategies.

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