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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)

Moreover, as with endogenous LCAC upregulation, exogenous LCAC delivery also induces spontaneous electrical arrhythmias, inhibits gap junction conductance, and promotes in vivo ventricular extra-systoles (see Figure 2B

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