ArticlePloS one2012
Protective effects of Acyl-coA thioesterase 1 on diabetic heart via PPARα/PGC1α signaling.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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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Who cites it
31 citing papers in PubMed, 47 citations in OpenAlex.
- Ferroptosis Signatures in Diabetic Cardiomyopathy: Multi-Omics Discovery and Validation of ACOT1 and TXNIP.Current issues in molecular biology · 2026Article
- ACOT1-specific expression modulates metabolic reprogramming in diabetic cardiomyopathy: The role of SREBP1c lactylation in CD36-mediated lipotoxicity.American heart journal plus : cardiology research and practice · 2026Article
- Acyl-CoA thioesterase 1 (ACOT1) overexpression alleviates heart failure by inhibiting oxidative stress and cardiomyocyte apoptosis through the Kelch-like ECH-associated protein1-NF-E2-related factor2 (KEAP1-NRF2) pathway.Experimental animals · 2026Article
- Acyl-CoA-binding protein as a driver of pathological aging.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- High fat diet feeding impairs neutrophil phagocytosis, bacterial killing, and neutrophil-induced hematopoietic regeneration.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Murine Model Insights: Identifying Dusp15 as a Novel Biomarker for Diabetic Cardiomyopathy Uncovered Through Integrated Omics Analysis and Experimental Validation.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Article
- Cyp2e1 knockdown attenuates high glucose-induced apoptosis and oxidative stress of cardiomyocytes by activating PI3K/Akt signaling.Acta diabetologica · 2023Article
- Acyl-Coa Thioesterases: A Rheostat That Controls Activated Fatty Acids Modulates Dengue Virus Serotype 2 Replication.Viruses · 2022Article
- The ThioesteraseOmics : a journal of integrative biology · 2021Article
- Identifying potential biomarkers of nonalcoholic fatty liver disease via genome-wide analysis of copy number variation.BMC gastroenterology · 2021Article
- Weighted Gene Co-Expression Network Analysis Identifies ANGPTL4 as a Key Regulator in Diabetic CardiomyopathyFrontiers in endocrinology · 2021Article
- The Universal Soldier: Enzymatic and Non-Enzymatic Antioxidant Functions of Serum Albumin.Antioxidants (Basel, Switzerland) · 2020Review
- Acyl-CoA thioesterase 1 prevents cardiomyocytes from Doxorubicin-induced ferroptosis via shaping the lipid composition.Cell death & disease · 2020Article
- Short high-fat diet interferes with the physiological maturation of the late adolescent mouse heart.Physiological reports · 2020Article
- Nuclear miR-320 Mediates Diabetes-Induced Cardiac Dysfunction by Activating Transcription of Fatty Acid Metabolic Genes to Cause Lipotoxicity in the Heart.Circulation research · 2019Article
- MiR-665 aggravates heart failure via suppressing CD34-mediated coronary microvessel angiogenesis.Aging · 2018Article
- Increasing Acyl CoA thioesterase activity alters phospholipid profile without effect on insulin action in skeletal muscle of rats.Scientific reports · 2018Article
- Indirect effect inference and application to GAW20 data.BMC genetics · 2018Article
- MiR-21 protected against diabetic cardiomyopathy induced diastolic dysfunction by targeting gelsolin.Cardiovascular diabetology · 2018Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundUsing fatty acids (FAs) exclusively for ATP generation was reported to contribute to the development of diabetic cardiomyopathy. We studied the role of substrate metabolism related genes in the heart of the diabetes to find out a novel therapeutic target for diabetic cardiomyopathy. METHODS AND
resultsBy microarray analysis of metabolic gene expression, acyl-CoA thioesterase 1 (acot1) was clearly upregulated in the myocardia of db/db mice, compared with normal control C57BL/Ks. Therefore, gain-of-function and loss-of-function approaches were employed in db/db mice to investigate the functions of ACOT1 in oxidative stress, mitochondrial dysfunction and heart function. We found that in the hearts of db/db mice which overexpressed ACOT1, H(2)O(2) and malondialdehyde (MDA) were reduced, the activities of ATPases in mitochondria associated with mitochondrial function were promoted, the expression of uncoupling protein 3 (UCP3) contributing to oxygen wastage for noncontractile purposes was decreased, and cardiac dysfunction was attenuated, as determined by both hemodynamic and echocardiographic detections. Consistently, ACOT1 deficiency had opposite effects, which accelerated the cardiac damage induced by diabetes. Notably, by real-time PCR, we found that overexpression of ACOT1 in diabetic heart repressed the peroxisome proliferator-activated receptor alpha/PPARγ coactivator 1α (PPARα/PGC1α) signaling, as shown by decreased expression of PGC1α and the downstream genes involved in FAs use.
conclusionOur results demonstrated that ACOT1 played a crucial protective role in diabetic heart via PPARα/PGC1α signaling.
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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.