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This signaling pathway is essential for the hypertrophic effects of IGF-1.23 Notably, IGF-1 has also been shown to promote intracellular lipid accumulation in mesangial cells, a phenotype similar to foam cells, which leads to reduced contractility in response to angiotensin-II.24,25 Furthermore, kidney samples from patients with advanced CKD and mouse models with renal fibrosis have defective fatty acid oxidation and higher lipid accumulation than controls without fibrosis

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