ReviewJournal of molecular endocrinology2015
Stress kinases in the modulation of metabolism and energy balance.
Review in Journal of molecular endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 76 citations in OpenAlex.
- Estradiol mitigates lipid accumulation, oxidative stress, apoptosis, and MAPKs activation in NASH rat model with bilateral orchidectomy.PNAS nexus · 2026Article
- Article
- Hepatic p38γ exacerbates acetaminophen‑induced acute liver injury via PI3K/Akt‑dependent mechanisms.International journal of molecular medicine · 2026Article
- CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026Review
- Article
- Comprehension of the Function of Antioxidants in Targeting Different Signaling Pathways to Cure Oxidative Stress-induced Hepatotoxicity.Current topics in medicinal chemistry · 2026Review
- p38α MAPK Regulation of Energy Metabolism in Skeletal Muscle Offers a Therapeutic Path for Type 2 Diabetes.Cells · 2025Review
- Exploring the Therapeutic Potential of TGF-β Inhibitors for Liver Fibrosis: Targeting Multiple Signaling Pathways.Journal of clinical and translational hepatology · 2025Review
- Excess Fructose Intake Activates Hyperinsulinemia and Mitogenic MAPK Pathways in Association With Cellular Stress, Inflammation, and Apoptosis in the Pancreas of Rats.Molecular nutrition & food research · 2025Article
- Fluorine-18-Labeled Positron Emission Tomography Probe Targeting Activated p38α: Design, Synthesis, and In Vivo Evaluation in Rodents.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Exploring the Therapeutic Potential of Glycyrrhiza Compounds in Alzheimer's Disease: A Comprehensive Review.Current topics in medicinal chemistry · 2025Review
- Licochalcone A: A Potential Multitarget Drug for Alzheimer's Disease Treatment.International journal of molecular sciences · 2023Review
- Article
- Experimental and Computational Investigation of the Oxime Bond Stereochemistry in c-Jun N-terminal Kinase 3 Inhibitors 11Pharmaceutics · 2023Article
- Article
- Metabolic Impact of MKP-2 Upregulation in Obesity Promotes Insulin Resistance and Fatty Liver Disease.Nutrients · 2022Article
- Article
- Identification of key genes and pathways revealing the central regulatory mechanism of brain-derived glucagon-like peptide-1 on obesity using bioinformatics analysis.Frontiers in neuroscience · 2022Article
- Article
- Regulation of the Golgi Apparatus by p38 and JNK Kinases during Cellular Stress Responses.International journal of molecular sciences · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Obesity is a new global pandemic, with growing incidence and prevalence. This disease is associated with increased risk of several pathologies, including diabetes, cardiovascular diseases, and cancer. The mechanisms underlying obesity-associated metabolic changes are the focus of efforts to identify new therapies. Stress-activated protein kinases (SAPK), including cJun N-terminal kinases (JNKs) and p38, are required for cellular responses to metabolic stress and therefore might contribute to the pathogenesis of obesity. Tissue-specific knockout models support a cell-type-specific role for JNK isoforms, in particular JNK1, highlighting its importance in cell homeostasis and organ crosstalk. However, more efforts are needed to elucidate the specific roles of other JNK isoforms and p38 family members in metabolism and obesity. This review provides an overview of the role of SAPKs in the regulation of metabolism.
Indexed as
Identifiers
What OpenQuestion holds
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.