ArticleThe Journal of biological chemistry2016
Small Molecular Allosteric Activator of the Sarco/Endoplasmic Reticulum Ca2+-ATPase (SERCA) Attenuates Diabetes and Metabolic Disorders.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.
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Who cites it
113 citing papers in PubMed, 190 citations in OpenAlex.
- Positive allosteric modulator of SERCA pump NDC-1171 attenuates cardiac functional decline in mouse model of Duchenne muscular dystrophy.Function (Oxford, England) · 2026Article
- Metabolic regulation of calcium homeostasis via SERCA succination.Science advances · 2026Article
- Failed metabolic adaptation to stress contributes to epidermal cell adhesion defects in Darier disease.Science advances · 2026Article
- Guardians of T-Cell CaCells · 2026Review
- Activation of sarco/endoplasmic reticulum Ca²⁺-ATPase 2 (SERCA2) reduces brain injury and improves cognitive function following ischemic stroke.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- Positive allosteric modulator of SERCA pump NDC-1171 attenuates cardiac functional decline in mouse model of Duchenne muscular dystrophy.bioRxiv : the preprint server for biology · 2026Article
- Supercharging the calcium pump: Identification of an activation hotspot on SERCA by cryo-EM.bioRxiv : the preprint server for biology · 2026Article
- The Landscape of SERCA2 in Cardiovascular Diseases: Expression Regulation, Therapeutic Applications, and Emerging Roles.Biomolecules · 2026Review
- Sarco/Endoplasmic Reticulum CaJournal of the American Heart Association · 2026Article
- The SERCA Pump: A Key Molecular Target in Calcium Handling of Vascular Smooth Muscle Cells in Metabolic Syndrome.Handbook of experimental pharmacology · 2026Review
- Small-Molecule Sarco/Endoplasmic Reticulum CaChemMedChem · 2026Article
- The SERCA-PLN-DWORF axis in cardiometabolic disease: mechanisms and therapeutic perspectives.Cardiovascular diabetology · 2025Review
- Pharmacological activation of SERCA2 reverses ER calcium dysregulation and depression-like behaviors in hyperglycemic mice.Scientific reports · 2025Article
- Unlocking the potential of atractylenolide II: Mitigating non-alcoholic fatty liver disease through farnesoid X receptor-endoplasmic reticulum stress interplay.Journal of pharmaceutical analysis · 2025Article
- Intracellular Calcium Dysregulation: The Hidden Culprit in the Diabetes-Gout Nexus.Biomedicines · 2025Review
- Gene and drug-mediated SERCA2a activation restores cardiac function and metabolic balance in diabetic mice.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Allosteric Modulation of SERCA Pumps in Health and Disease: Structural Dynamics, Posttranslational Modifications, and Therapeutic Potential.Journal of molecular biology · 2025Review
- A Small-Molecule Activator of Sarco/Endoplasmic Reticulum CaACS pharmacology & translational science · 2025Article
- SERCA blockade as a treatment strategy for obesity.European journal of applied physiology · 2025Review
- Rapamycin Alleviates Heart Failure Caused by Mitochondrial Dysfunction and SERCA Hypoactivity in Syntaxin 12/13 Deficient Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
53 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Dysregulation of endoplasmic reticulum (ER) Ca(2+) homeostasis triggers ER stress leading to the development of insulin resistance in obesity and diabetes. Impaired function of the sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA) has emerged as a major contributor to ER stress. We pharmacologically activated SERCA2b in a genetic model of insulin resistance and type 2 diabetes (ob/ob mice) with a novel allosteric activator, CDN1163, which markedly lowered fasting blood glucose, improved glucose tolerance, and ameliorated hepatosteatosis but did not alter glucose levels or body weight in lean controls. Importantly, CDN1163-treated ob/ob mice maintained euglycemia comparable with that of lean mice for >6 weeks after cessation of CDN1163 administration. CDN1163-treated ob/ob mice showed a significant reduction in adipose tissue weight with no change in lean mass, assessed by magnetic resonance imaging. They also showed an increase in energy expenditure using indirect calorimetry, which was accompanied by increased expression of uncoupling protein 1 (UCP1) and UCP3 in brown adipose tissue. CDN1163 treatment significantly reduced the hepatic expression of genes involved in gluconeogenesis and lipogenesis, attenuated ER stress response and ER stress-induced apoptosis, and improved mitochondrial biogenesis, possibly through SERCA2-mediated activation of AMP-activated protein kinase pathway. The findings suggest that SERCA2b activation may hold promise as an effective therapy for type-2 diabetes and 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.