RESUMEN
Evidence suggests severe coronavirus disease-19 (COVID-19) infection is characterised by pulmonary and systemic microvasculature dysfunction, specifically, acute endothelial injury, hypercoagulation and increased capillary permeability. Diabetes, which is also characterised by vascular injury in itself, confers an increased risk of adverse COVID-19 outcomes. It has been suggested that pre-existing endothelial dysfunction and microvascular disease in diabetes will exacerbate the vascular insults associated with COVID-19 and thus lead to increased severity of COVID-19 infection. In this article, we evaluate the current evidence exploring the impact of microvascular complications, in the form of diabetic retinopathy and nephropathy, in individuals with COVID-19 and diabetes. Future insights gained from exploring the microvascular injury patterns and clinical outcomes may come to influence care delivery algorithms for either of these conditions.
Asunto(s)
COVID-19/fisiopatología , Angiopatías Diabéticas/fisiopatología , Endotelio Vascular/patología , Microcirculación , Pandemias , SARS-CoV-2 , Trombofilia/etiología , Albuminuria/etiología , COVID-19/complicaciones , Permeabilidad Capilar , Atención a la Salud , Angiopatías Diabéticas/complicaciones , Nefropatías Diabéticas/complicaciones , Nefropatías Diabéticas/fisiopatología , Neuropatías Diabéticas/complicaciones , Neuropatías Diabéticas/fisiopatología , Retinopatía Diabética/complicaciones , Retinopatía Diabética/fisiopatología , Endotelio Vascular/lesiones , Humanos , Obesidad/complicaciones , Obesidad/fisiopatología , Circulación Pulmonar , Edema Pulmonar/etiología , Edema Pulmonar/fisiopatología , Índice de Severidad de la Enfermedad , Trombofilia/fisiopatología , Resultado del TratamientoRESUMEN
Toll-like receptor 4 (TLR4) contributes to the pathophysiology of diabetes. This happens, at least in part, because TLR4 modulates the enzyme NADPH oxidase, a primary source of ROS in vascular structures. Increased oxidative stress disrupts key vascular signaling mechanisms and drives the progression of diabetes, elevating the likelihood of cardiovascular diseases. Recently, it has been shown that patients with diabetes are also at a higher risk of developing severe coronavirus disease 2019 (COVID-19). Given the importance of the interaction between TLR4 and NADPH oxidase to the disrupted diabetic vascular system, we put forward the hypothesis that TLR4-mediated NADPH oxidase-derived ROS might be a critical mechanism to help explain why this disparity appears in diabetic patients, but unfortunately, conclusive experimental evidence still lacks in the literature. Herein, we focus on discussing the pathological implications of this signaling communication in the diabetic vasculature and exploring this crosstalk in the context of diabetes-associated severe COVID-19.