ArticleNature metabolism2019
Dysregulation of Amyloid Precursor Protein Impairs Adipose Tissue Mitochondrial Function and Promotes Obesity.
Article in Nature metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 71 citations in OpenAlex.
- Molecular Mechanisms of Obesity-Associated Oxidative Stress and Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Tagged and untagged amyloid precursor protein E2 domain have comparable thermal stability and metal-ion binding propensity.BMC research notes · 2026Article
- Article
- Unrestrained fatty acid oxidation triggers heart failure in mice via cardiolipin loss and mitochondrial dysfunction.The Journal of clinical investigation · 2026Article
- Amyloid precursor protein interacts with the mitochondrial phosphatase PGAM5 and regulates mitochondrial respiration.bioRxiv : the preprint server for biology · 2026Article
- Unrestrained fatty acid oxidation triggers heart failure in mice via cardiolipin loss and mitochondrial dysfunction.bioRxiv : the preprint server for biology · 2026Article
- Altered mitochondrial functionality in metabolic disorders: insights fromFrontiers in endocrinology · 2026Review
- The impact of low carbohydrate diet on the plasma proteomic profile of individuals with obesity.Frontiers in nutrition · 2026Article
- Adipogenin promotes the development of lipid droplets by binding a dodecameric seipin complex.Science (New York, N.Y.) · 2025Article
- Hippo-YAP/TAZ-ROS signaling axis regulates metaflammation induced by SelenoM deficiency in high-fat diet-derived obesity.Journal of advanced research · 2025Article
- Mitochondrial protein import stress.Nature cell biology · 2025Review
- Subclinical ketosis in postpartum dairy cows alters the adipose tissue immunological profile in a depot-specific manner.Frontiers in immunology · 2025Article
- The mTOR Pathway: A Common Link Between Alzheimer's Disease and Down Syndrome.Journal of clinical medicine · 2024Review
- Article
- Protocol for Seahorse analysis of ex vivo mouse brown and white adipose tissues.STAR protocols · 2024Article
- Amyloid beta 42 alters cardiac metabolism and impairs cardiac function in male mice with obesity.Nature communications · 2024Article
- Navigating the landscape of mitochondrial-ER communication in health and disease.Frontiers in molecular biosciences · 2024Review
- The Emerging Importance of Mitochondria in White Adipocytes: Neither Last nor Least.Endocrinology and metabolism (Seoul, Korea) · 2023Article
- Proteolytic rewiring of mitochondria by LONP1 directs cell identity switching of adipocytes.Nature cell biology · 2023Article
- Controversial Properties of Amyloidogenic Proteins and Peptides: New Data in the COVID Era.Biomedicines · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
Mitochondrial function in white adipose tissue (WAT) is an important yet understudied aspect in adipocyte biology. Here, we report a role for amyloid precursor protein (APP) in compromising WAT mitochondrial function through a high-fat diet (HFD)-induced, unconventional mis-localization to mitochondria that further promotes obesity. In humans and mice, obese conditions significantly induce APP production in WAT and its enrichment in mitochondria. Mechanistically, a HFD-induced dysregulation of signal recognition particle subunit 54c is responsible for the mis-targeting of APP to adipocyte mitochondria. Mis-localized APP blocks the protein import machinery, leading to mitochondrial dysfunction in WAT. Adipocyte-specific and mitochondria-targeted APP overexpressing mice display increased body mass and reduced insulin sensitivity, along with dysfunctional WAT due to a dramatic hypertrophic program in adipocytes. Elimination of adipocyte APP rescues HFD-impaired mitochondrial function with significant protection from weight gain and systemic metabolic deficiency. Our data highlights an important role of APP in modulating WAT mitochondrial function and obesity-associated metabolic dysfunction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.