Taurine for COVID-19

Sirtuin 1 (SIRT1) is a crucial regulator of cellular processes, including inflammation, metabolism, and stress responses, playing a significant role in the body′s defense mechanisms. During SARS‐CoV‐2 infection, SIRT1 plays a crucial role in modulating the immune response. This protein helps to enhance the antiviral response through deacetylating key transcription factors and regulating proinflammatory cytokines, thereby reducing the cytokine storm (an overwhelming immune response) associated with severe COVID‐19 cases. SIRT1 influences the expression of angiotensin‐converting enzyme 2 (ACE2), the primary receptor for SARS‐CoV‐2, thereby potentially mitigating viral entry and replication. Natural activators of SIRT1, such as resveratrol, have been shown to enhance its activity, offering promising avenues for therapeutic interventions aimed at bolstering the immune response during COVID‐19. Understanding the multifaceted role of SIRT1 in human defense mechanisms against SARS‐CoV‐2 could pave the way for innovative strategies to manage COVID‐19 and similar viral infections, emphasizing the importance of SIRT1 as a potential target for future therapeutic approaches.

AbstractAcute respiratory distress syndrome (ARDS) is a common condition associated with critically ill patients, characterized by bilateral chest radiographical opacities with refractory hypoxemia due to noncardiogenic pulmonary edema. Despite significant advances, the mortality of ARDS remains unacceptably high, and there are still no effective targeted pharmacotherapeutic agents. With the outbreak of coronavirus disease 19 worldwide, the mortality of ARDS has increased correspondingly. Comprehending the pathophysiology and the underlying molecular mechanisms of ARDS may thus be essential to developing effective therapeutic strategies and reducing mortality. To facilitate further understanding of its pathogenesis and exploring novel therapeutics, this review provides comprehensive information of ARDS from pathophysiology to molecular mechanisms and presents targeted therapeutics. We first describe the pathogenesis and pathophysiology of ARDS that involve dysregulated inflammation, alveolar-capillary barrier dysfunction, impaired alveolar fluid clearance and oxidative stress. Next, we summarize the molecular mechanisms and signaling pathways related to the above four aspects of ARDS pathophysiology, along with the latest research progress. Finally, we discuss the emerging therapeutic strategies that show exciting promise in ARDS, including several pharmacologic therapies, microRNA-based therapies and mesenchymal stromal cell therapies, highlighting the pathophysiological basis and the influences on signal transduction pathways for their use.