ArticleEMBO reports2018
CLPP deficiency protects against metabolic syndrome but hinders adaptive thermogenesis.
Article in EMBO reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 54 citations in OpenAlex.
- Pharmacological inhibition of CLPP stabilizes LETMD1 to boost thermogenesis and alleviate obesity.Adipocyte · 2026Article
- CLPP loss confers sex-specific protection from renal ischemia reperfusion injury.Redox biology · 2026Article
- Targeting ClpP Protease: Emerging Therapeutic Strategies and Small-Molecule Modulators in Drug Discovery.Medicinal research reviews · 2026Review
- Exercise elicits mitonuclear protein imbalance and UPRJournal of physiology and biochemistry · 2026Article
- Molecular mechanisms of mitochondrial AAA+ proteases.The Journal of biological chemistry · 2026Review
- ClpP deficiency attenuates contrast-induced HK-2 cell injury through changes associated with mitochondrial dynamics and apoptosis.PloS one · 2026Article
- 2-hydroxyglutarate mediates whitening of brown adipocytes coupled to nuclear softening upon mitochondrial dysfunction.Nature metabolism · 2025Article
- Recent Advances in the Structural Studies of the Proteolytic ClpP/ClpX Molecular Machine.Biomolecules · 2025Review
- CLPP Gene Variants Causing Perrault Syndrome Type 3 in Han Chinese Families: A Genotype-Phenotype Study.Human genomics · 2025Article
- Mipep deficiency in adipocytes impairs mitochondrial protein maturation and leads to systemic inflammation and metabolic dysfunctions.Scientific reports · 2025Article
- Deletion of miPEP in adipocytes protects against obesity and insulin resistance by boosting muscle metabolism.Molecular metabolism · 2024Article
- Review
- CLPP-Null Eukaryotes with Excess Heme Biosynthesis Show Reduced L-arginine Levels, Probably via CLPX-Mediated OAT Activation.Biomolecules · 2024Article
- Loss of Mfn1 but not Mfn2 enhances adipogenesis.PloS one · 2024Article
- A coordinated multiorgan metabolic response contributes to human mitochondrial myopathy.EMBO molecular medicine · 2023Article
- Exercise Induces an Augmented Skeletal Muscle Mitochondrial Unfolded Protein Response in a Mouse Model of Obesity Produced by a High-Fat Diet.International journal of molecular sciences · 2023Article
- Reduced insulin signaling in neurons induces sex-specific health benefits.Science advances · 2023Article
- OxPhos defects cause hypermetabolism and reduce lifespan in cells and in patients with mitochondrial diseases.Communications biology · 2023Article
- Mitochondrial proteostasis stress in muscle drives a long-range protective response to alleviate dietary obesity independently of ATF4.Science advances · 2022Article
- FGF21 modulates mitochondrial stress response in cardiomyocytes only under mild mitochondrial dysfunction.Science advances · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria are fundamental for cellular metabolism as they are both a source and a target of nutrient intermediates originating from converging metabolic pathways, and their role in the regulation of systemic metabolism is increasingly recognized. Thus, maintenance of mitochondrial homeostasis is indispensable for a functional energy metabolism of the whole organism. Here, we report that loss of the mitochondrial matrix protease CLPP results in a lean phenotype with improved glucose homeostasis. Whole-body CLPP-deficient mice are protected from diet-induced obesity and insulin resistance, which was not present in mouse models with either liver- or muscle-specific depletion of CLPP However, CLPP ablation also leads to a decline in brown adipocytes function leaving mice unable to cope with a cold-induced stress due to non-functional adaptive thermogenesis. These results demonstrate a critical role for CLPP in different metabolic stress conditions such as high-fat diet feeding and cold exposure providing tools to understand pathologies with deregulated
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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.