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However, more large, randomized controlled studies are needed in this direction
Their advantage lies in the ability to sensitively capture the early cascade of events, ranging from impaired mitochondrial fatty acid oxidation to transport defects and tubular metabolic imbalance, thereby complementing the molecular trajectory of DKD that is not adequately reflected by conventional UACR measurements (Table 1)
Any medication adjustments, including changes to the tirzepatide dose or titration schedule, should be made under healthcare provider guidance based on overall tolerability and treatment goals
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HMGB1 can also be considered as an alarmin in myocardial tissues which exacerbates the pathological characteristics involving DCM by inducing the release of cytokines, promoting chemotaxis of immune cells, activating immune cells, endothelial cells and fibroblasts and serving as an adjuvant in the production of autoantibodies
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