Fig. 3.

Therapeutic potential of targeting TLR4 and P2X7 signaling in COVID–19–induced hyperinflammation. SARS-CoV-2 infection activates TLR4 and P2X7 on alveolar macrophages, triggering downstream inflammatory cascades via NF-κB and inflammasome activation. This results in the release of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α, contributing to cytokine storm and acute respiratory distress syndrome (ARDS). Pharmacological inhibition of TLR4 and P2X7 may attenuate these responses, reduce pulmonary inflammation, and prevent severe lung damage in COVID-19 patients