Plasma profiling of COVID-19 patients revealed significantly elevated sACE2 and Ang II compared to controls, with Ang II associated with oxygen supplementation and dyspnea.
Observational
Acute COVID-19 disrupts the RAAS system, with elevated Ang II linked to respiratory compromise and specific cytokine alterations, highlighting its potential as a biomarker.
COVID-19 perturbs the renin-angiotensin system (RAAS) and inflammatory pathways, shaping disease severity. Soluble ACE2 (sACE2) and angiotensin II (Ang II) are central regulators of vascular and immune homeostasis. We profiled plasma from COVID-19 patients and controls using ELISA, together with 48 cytokine profiling and clinical data. Both sACE2 and Ang II were significantly elevated in patients. Increased Ang II was associated with oxygen supplementation and dyspnea, and negatively correlated with IL-3, whereas sACE2 correlated with IL-13 and FGF. Comorbidities modulated cytokine expression: diabetes mellitus was linked to reduced LIF and MCP-1, hypertension to decreased LIF and increased IP-10, and obesity to elevated IL-12p70. Age correlated with TNF and HGF, and reduced oxygen saturation was associated with lower LIF. These findings reveal that acute COVID-19 disrupts RAAS and amplifies immune dysregulation, with Ang II emerging as a pivotal mediator of respiratory compromise and inflammatory imbalance, underscoring its potential as a biomarker and therapeutic relevance.
Fernandes et al. (Fri,) conducted a observational in COVID-19. Plasma profiling vs. Controls was evaluated on Plasma levels of sACE2, Ang II, and cytokines. Plasma profiling of COVID-19 patients revealed significantly elevated sACE2 and Ang II compared to controls, with Ang II associated with oxygen supplementation and dyspnea.
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