Diabetic endothelial microangiopathy and pulmonary dysfunction

Abstract

Type 2 diabetes mellitus (T2DM) is a widespread metabolic condition with a high global morbidity and mortality rate that affects the whole body. Their primary consequences are mostly caused by the macrovascular and microvascular bed degradation brought on by metabolic, hemodynamic, and inflammatory variables. However, research in recent years has expanded the target organ in T2DM to include the lung. Inflammatory lung diseases also impose a severe financial burden on global healthcare. T2DM has long been recognized as a significant comorbidity that influences the course of various respiratory disorders and their disease progress. The pathogenesis of the glycemic metabolic problem and endothelial microangiopathy of the respiratory disorders have garnered more attention lately, indicating that the two ailments have a shared history. This review aims to outline the connection between T2DM related endothelial cell dysfunction and concomitant respiratory diseases, including Coronavirus disease 2019 (COVID-19), asthma, chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF).

Evaluation of bi-directional causal association between obstructive sleep apnoea syndrome and diabetic microangiopathy: a Mendelian randomization study

“…This is the fundamental cause of diabetic microvascular complications ( 81 ). At the same time, reductions in FVC and FEV1 are correlated with increased levels of Hypoxia-Inducible Factor-1 (HIF-1) and VEGF ( 51 ), thereby heightening the likelihood of endothelial vascular lesions related to diabetes.…”

Persistent Hyperglycemia Worsens the Oleic Acid Induced Acute Lung Injury in Rat Model of Type II Diabetes Mellitus

“…[ 3 ] Additionally, in individuals with diabetes, lung endothelial dysfunction and thickening of the interstitial lung layer may be caused by chronic systemic inflammation linked to oxidative stress and loss of antioxidant capacity. [ 33 , 34 ] According to recent research, NADPH oxidase or the polyol pathway activation may be the mechanism causing diabetic lung damage. [ 3 , 34 ] In hyperglycemia, a rise in the STAT3 (‘Signal Transducer and Activator of Transcription 3’) genes also contributes to cell injury.…”

“…[ 33 , 34 ] According to recent research, NADPH oxidase or the polyol pathway activation may be the mechanism causing diabetic lung damage. [ 3 , 34 ] In hyperglycemia, a rise in the STAT3 (‘Signal Transducer and Activator of Transcription 3’) genes also contributes to cell injury. [ 4 , 34 ] At the same time, the cellular mechanisms for these abnormalities are still unclear.…”

“…[ 3 , 34 ] In hyperglycemia, a rise in the STAT3 (‘Signal Transducer and Activator of Transcription 3’) genes also contributes to cell injury. [ 4 , 34 ] At the same time, the cellular mechanisms for these abnormalities are still unclear.…”

Relationship between subclinical hypothyroidism and endothelial dysfunction in patients with type 2 diabetes: A cross-sectional study

“…Endothelial dysfunction, as a hallmark of generalized microangiopathy in humans, is not only a key node in the occurrence of a series of cardiovascular diseases but also a trait stage of diabetes that can in uence the pathophysiology of diabetic vasculopathy and ultimately lead to clinical CVD [6][7][8]. The recent evidence on the relationship between SCH and endothelial dysfunction [7,9] suggests that careful attention must be paid to endothelial function early, especially in T2DM patients with SCH. In the past few years, non-invasive indicators of endothelial dysfunction that e ciently assess early vascular changes have increasingly attracted the interest of researchers.…”