Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance and progressive β-cell dysfunction, resulting in persistent hyperglycemia and long-term vascular complications. The global prevalence of T2DM continues to rise and is strongly associated with cardiovascular disease, chronic kidney disease, and the broader cardiovascular–kidney–metabolic (CKM) syndrome. This review summarizes the pathophysiology of T2DM, with emphasis on insulin resistance, endothelial dysfunction, oxidative stress, and activation of the renin–angiotensin–aldosterone system, all of which contribute to progressive end-organ damage. Chronic hyperglycemia further promotes inflammatory and fibrotic pathways that accelerate diabetic kidney disease and atherosclerotic cardiovascular disease. Finerenone, a non-steroidal mineralocorticoid receptor antagonist, has emerged as a therapeutic option for patients with T2DM and chronic kidney disease. Clinical trial data demonstrate that finerenone reduces albuminuria and provides cardiovascular and renal protection by reducing inflammation and fibrosis. Its use is associated with a generally acceptable safety profile, although hyperkalemia remains an important adverse effect requiring routine monitoring. Overall, T2DM is a multifactorial disease that requires comprehensive management targeting metabolic dysregulation as well as inflammatory and hormonal pathways. Finerenone represents an important advancement in cardiorenal protection. Understanding the interconnected mechanisms underlying CKM syndrome is essential for improving longterm outcomes in individuals with T2DM.