tetano
Editor, Senior Moderator
Cytokine
. 2026 Sep 1:207:157209.
doi: 10.1016/j.cyto.2026.157209. Online ahead of print.
Aline Borges BarbosaTeles 1 , Larisse de Souza Barbosa Lacerda 2 , Rafael Ferreira Calil 1 , Celso Martins Queiroz-Junior 2 , Ana Flávia Santos Linhares 1 , Mauro Martins Teixeira 3 , Marina Gomes Miranda E Castor 1 , Vivian Vasconcelos Costa 2 , Stefany Cau 4
Affiliations
Coronavirus diseases, particularly COVID-19, been associated with cardiac injury. Given that obesity is a well-known risk factor for severe cases with poorer outcomes, we hypothesized that cardiac involvement in a murine betacoronavirus infection would be exacerbated in pre-obese mice. To test this hypothesis, we fed mice a short-term (4-week) cafeteria diet (Caf), which resulted in increased body fat and mild cardiac histological damage, myocyte hypertrophy and fibrosis. Following the diet, we performed intranasal infection with MHV-A59 and evaluated the lungs and hearts eight days post-infection. In the lungs, infection was acute, caused moderate lung injury and was self-limited in both Chow-fed and Caf-fed mice with similar low viral loads recovered from this tissue. Meanwhile, cardiac fibrosis was significantly exacerbated in the Caf diet mice infected with MHV-A59. We also observed elevated levels of circulating cytokines, TNF and IL-10, as well as increased cardiac oxidative stress, solely in the obese infected mice. In contrast, isolated hearts from lean infected mice showed an increased response to β-adrenergic stimulation, which was damped in the Caf diet infected group. These findings indicate that obesity is a significant risk factor for cardiac issues caused by coronavirus infection by modulating local oxidative stress and systemic inflammation.
Keywords: Betacoronavirus; Cafeteria diet; Heart fibrosis; Oxidative stress; Systemic inflammation.
. 2026 Sep 1:207:157209.
doi: 10.1016/j.cyto.2026.157209. Online ahead of print.
Obesity exacerbates cardiac oxidative stress and fibrosis upon coronavirus infection
Aline Borges BarbosaTeles 1 , Larisse de Souza Barbosa Lacerda 2 , Rafael Ferreira Calil 1 , Celso Martins Queiroz-Junior 2 , Ana Flávia Santos Linhares 1 , Mauro Martins Teixeira 3 , Marina Gomes Miranda E Castor 1 , Vivian Vasconcelos Costa 2 , Stefany Cau 4
Affiliations
- PMID: 42685505
- DOI: 10.1016/j.cyto.2026.157209
Abstract
Coronavirus diseases, particularly COVID-19, been associated with cardiac injury. Given that obesity is a well-known risk factor for severe cases with poorer outcomes, we hypothesized that cardiac involvement in a murine betacoronavirus infection would be exacerbated in pre-obese mice. To test this hypothesis, we fed mice a short-term (4-week) cafeteria diet (Caf), which resulted in increased body fat and mild cardiac histological damage, myocyte hypertrophy and fibrosis. Following the diet, we performed intranasal infection with MHV-A59 and evaluated the lungs and hearts eight days post-infection. In the lungs, infection was acute, caused moderate lung injury and was self-limited in both Chow-fed and Caf-fed mice with similar low viral loads recovered from this tissue. Meanwhile, cardiac fibrosis was significantly exacerbated in the Caf diet mice infected with MHV-A59. We also observed elevated levels of circulating cytokines, TNF and IL-10, as well as increased cardiac oxidative stress, solely in the obese infected mice. In contrast, isolated hearts from lean infected mice showed an increased response to β-adrenergic stimulation, which was damped in the Caf diet infected group. These findings indicate that obesity is a significant risk factor for cardiac issues caused by coronavirus infection by modulating local oxidative stress and systemic inflammation.
Keywords: Betacoronavirus; Cafeteria diet; Heart fibrosis; Oxidative stress; Systemic inflammation.