Vascular Immune Crosstalk in COVID-19: RAAS Biomarker Signature Linking Angiotensin II to Respiratory Compromise and Soluble ACE2 to IL-13 and FGF, Revealing Therapeutic Targets
Year: 2026
Type: article
Study design: Observational Study
Abstract: 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.
DOI: 10.3390/ijms27083579
Authors: Thais Freitas Barreto Fernandes, Itauá Leston Araujo, Pedro Henrique Oliveira Vianna, Adriana Cesar Bonomo, José Henrique Pilotto, Fernanda Heloise Côrtes, Mariza Gonçalves Morgado, Carmem Beatriz Wagner Giacoia-Gripp, Nathalia Beatriz Ramos De Sá, Marcelo Ribeiro-Alves, Maria Pia Diniz Ribeiro, Sandra Wagner Cardoso, Valdilea G. Veloso, Beatriz Grinsztejn, Roberto Magalhães Saraiva, Dalziza Victalina De Almeida
Institution: Fundação Oswaldo Cruz
Language: English
Subfield: Infectious Diseases
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,499
Funder: Fundação Oswaldo Cruz
Awards: G5694355386, G5860089425, G6280557379
OpenAlex ID: W7154753790
