ArticleCells2026
Diet-Induced Amyloid Precursor Protein Dysregulation in Kidney and Adipose Tissue Mediates Mitochondrial Dysfunction.
Article in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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4 authors.
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Abstract
While amyloid precursor protein (APP) overexpression in adipose tissue is a recognized consequence of high-fat diet (HFD) feeding, its role in metabolically active organs and the mechanisms linking it to systematic dysfunction remain unclear. In particular, the potential for diet-induced APP dysregulation in the other tissues and the contribution of its βC-terminal fragment (βCTF) are poorly characterized. Using a high-fat diet (HFD) mouse model to induce systematic metabolic stress, we assessed APP and βCTF levels across multiple tissues. HFD triggered a tissue-specific response, with APP levels increasing >2-fold in visceral and subcutaneous white adipose tissue (WAT) and in the kidney but remained unchanged in the liver and brain. βCTF levels were significantly elevated in the visceral WAT (3-fold) and kidney. In these responsive tissues, APP and βCTF accumulated within mitochondria, which coincided with significantly reduced complex I and IV activities. Complementary in vitro studies confirmed that APP levels can dictate mitochondrial function. Furthermore, we identified that cytokines-IL-4, IL-13, TNF-α, and IL-1β-induced
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