UCP3

Last update 08 May 2025

Basic Info

Synonyms

Mitochondrial uncoupling protein 3, SLC25A9, Solute carrier family 25 member 9

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Introduction

Putative transmembrane transporter that plays a role in mitochondrial metabolism via an as yet unclear mechanism (PubMed:21775425, PubMed:36114012). Originally, this mitochondrial protein was thought to act as a proton transmembrane transporter from the mitochondrial intermembrane space into the matrix, causing proton leaks through the inner mitochondrial membrane, thereby uncoupling mitochondrial membrane potential generation from ATP synthesis (PubMed:11171965, PubMed:12670931, PubMed:12734183, PubMed:9305858). However, this function is controversial and uncoupling may not be the function, or at least not the main function, but rather a consequence of more conventional metabolite transporter activity (PubMed:11707458).

100 Clinical Results associated with UCP3

100 Translational Medicine associated with UCP3

0 Patents (Medical) associated with UCP3

1,562

Literatures (Medical) associated with UCP3

01 May 2025·Journal of Molecular and Cellular Cardiology

Uncoupling protein 3 protects against pathological cardiac hypertrophy via downregulation of aspartate

Article

Author: Liu, Shenyan ; Yang, Huang-Tian ; Yin, Huiyong ; Tan, Jiliang ; Shan, Huitong ; Wang, Yajun ; Li, Xuxia ; Li, Luxiao

Metabolic remodeling involving alterations in the substrate utilization is a key feature of cardiac hypertrophy. However, the molecular mechanisms underlying regulation of tricarboxylic acid cycle intermediates by mitochondrial membrane proteins during cardiac hypertrophy have not yet been fully clarified. Mitochondrial uncoupling protein 3 (UCP3), an anion transporter located on the inner mitochondrial membrane, exerts cardioprotective effects against ischemia/reperfusion injury and its insufficiency exacerbates left ventricular (LV) diastolic dysfunction during hypertension. However, its role in pressure overload-induced cardiac hypertrophy remains unknown. Here, we found that UCP3 was downregulated in the mouse LV with transverse aortic constriction (TAC)-induced pathological hypertrophy and in phenylephrine (PE)-stimulated hypertrophic neonatal rat cardiomyocytes (NRCMs). The TAC-induced hypertrophy and LV dysfunction were aggravated in global and cardiac specific knockout of UCP3 (UCP3cKO) mice but improved by cardiac specific overexpression of UCP3 (UCP3cOE). Similar alterations in hypertrophy were observed in PE-treated NRCMs with UCP3-knockdown/overexpression. Moreover, the TAC-increased aspartate and glutamic-oxaloacetic transaminase 2 (GOT2) activity were enhanced in UCP3cKO hearts but reversed in UCP3cOE ones. PE-induced increases of GOT2 activity were enhanced in the UCP3-knockdown NRCMs but attenuated in the UCP3 overexpression ones, accompanied with the downregulation of aspartate. The endogenous interaction of UCP3 and GOT2 was weakened in the PE-treated NRCMs compared with the PE-untreated cells. Furthermore, aspartate supplementation reversed the UCP3 overexpression-attenuated hypertrophy in the PE-stimulated NRCMs. In conclusion, UCP3 expression is downregulated in hypertrophic hearts and cardiomyocytes, whereas the increase of UCP3 mitigates cardiac hypertrophy by downregulation of the enhanced aspartate. These findings provide new knowledge for the function of UCP3 and therapeutic target for cardiac hypertrophy.

01 May 2025·Naunyn-Schmiedeberg's Archives of Pharmacology

Evaluation of the toxicity potential of exercise and atorvastatin/metformin combination therapy on STZ-diabetic rats

Article

Author: Tunçyürekli, Merve ; Tülüce, Yasin ; Erciyas, Ferzan Lermioglu

Exercise is recommended for individuals with diabetes, and metformin and atorvastatin are commonly prescribed to diabetic patients. However, these two drugs have potential effects that may lead to toxicity in the skeletal muscle system. Therefore, the effects and potential interactions of combining these two drugs on skeletal muscle performance and structure were investigated in vivo in an experimental diabetes model. Male Wistar rats were divided into six groups: a sedentary control group (N) and five treatment groups-exercise (C), diabetes (D), diabetes with metformin (MET), diabetes with atorvastatin (ATO), and diabetes with metformin and atorvastatin (MET + ATO). In the diabetes model experimentally created with streptozotocin (STZ; 45 mg/kg, i.p.) and metformin (300 mg/kg/day), atorvastatin (10 mg/kg/day) was administered to drug groups by gavage during the 4-week study period. The rats were allowed to run (at moderate level) for 30 min, 5 days a week, on the treadmill. At the end of the study, blood samples and gastrocnemius muscle tissues of the rats were obtained under ketamine anesthesia (100 mg/kg; i.p). The effects of combining exercise and medication on skeletal muscle were assessed by examining the levels of significant biomarkers including PGC-1α, UCP-3, and MyHCs, as well as analyzing oxidative stress/antioxidant capacity parameters in muscle tissue samples. Additionally, relevant biochemical indicators were determined in serum samples. The quantity and morphology of mitochondria in muscle tissue were assessed using transmission electron microscopy. It was observed in the study that some toxic effects associated with the use of drugs alone were reduced by combination therapy. It is thought that this study will contribute to the literature in the evaluation of the effects of drugs and their combined use in Type 1 diabetes under exercise conditions.

01 Apr 2025·Obesity Research & Clinical Practice

Persian Gulf brown seaweed extracts showing anti-obesity potency on adipogenic differentiation in human adipose-derived mesenchymal stem cells and obese male rats

Article

Author: Tanideh, Nader ; Taherizadeh, Mohammreza ; Rahmani-Moghadam, Ebrahim ; Talaei-Khozani, Tahereh ; Zarrin, Vahideh

The objectives of this study were to compare the effects of two Persian Gulf marine algae, Padina pavonica (Pp) and Sargassum angustifolium (Sa), on both in vitro and in vivo models. Hot water and Ethanolic extracts of Pp (HWE.Pp, EE.Pp) and Sa (HWE.Sa, EE.Sa) were added to human adipose-derived mesenchymal stem cells (hADMSCs) cultures treated with adipogenic medium. An in vivo study was done by feeding the extracts to the high-fat diet (HFD) male Wistar rats. A decrease in adipocyte differentiation, and an increase in leptin production and energy loss as indicated by UCP1 and UCP3 upregulation and intracellular glucose content were detected. Weight loss, food intake reduction, downregulation of the PPARγ, and upregulation of UCP1, UCP3, FNDC5, and leptin were observed in the animals were fed with both algae compared to untreated obese and normal rats. Both extracts with superiority of Sa also normalized the level of blood sugar, cholesterol, triglyceride, low-density lipoprotein (LDL), high-density lipoprotein (HDL), as well as inflammatory factors and liver enzymes. HW-Sa was the best extract to normalize all the criteria. Sa can be considered as a good remedy for losing weight by inhibiting adipocyte differentiation, and inflammation, increasing energy loss, and decreasing food intake through leptin elevation.

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UCP3

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