Type 2 Diabetes and Oxidative Stress and Inflammation: Pathophysiological Mechanisms and Possible Therapeutic Options

Type 2 diabetes (T2D) is a public health burden associated with high healthcare and societal costs and elevated morbidity and mortality [1]. The number of T2D patients has quadrupled in the past three decades, and this disease represents the ninth major cause of death [2]. In addition to a correct lifestyle, including maintaining a healthy body weight, a proper diet, physical activity, not smoking/smoking cessation, and traditional pharmacological interventions (e.g., insulin, metformin), newer diabetes mellitus drug classes, i.e., sodium-glucose transport protein 2 (SGLT2) inhibitors and Glucagon-Like Peptide-1 Receptor Agonists (GLP-1Ras) are recommended in recent guidelines as the add-on therapy to metformin to improve glycaemic control [3]. These pharmacological agents are particularly advantageous for patients with cardiovascular disease, as these drugs also retain cardiovascular benefits that appear independent of glycaemic control and of baseline metformin use [4,5]. There is strong evidence of interrelationships between oxidative stress and inflammation and molecular and cellular events related to T2D onset, progression, and complications [6,7]. Interestingly, different agents may target inflammatory and pro-oxidant pathways related to T2D, providing additional potential therapeutic benefits for the treatment of T2D [8]. Five research studies addressed different aspects of this important topic in this Special Issue.