ReviewDiabetologia2016
IRS proteins and diabetic complications.
Review in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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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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.
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Who cites it
50 citing papers in PubMed, 109 citations in OpenAlex.
- ClinASO: An open-source platform for rapid drug discovery of gapmer antisense oligonucleotides.Molecular therapy. Nucleic acids · 2026Article
- Biochemical-Cellular crosstalk in diabetes: exploring pathways driving microvascular complications.Molecular biology reports · 2026Review
- The Complex Gene-Carbohydrate Interaction in Type 2 Diabetes: Between Current Knowledge and Future Perspectives.Nutrients · 2025Review
- Exploration of the shared gene signatures and molecular mechanisms between cardioembolic stroke and ischemic stroke.Frontiers in neurology · 2025Article
- Research progress on the association of insulin resistance with type 2 diabetes mellitus and Alzheimer's disease.Metabolic brain disease · 2024Review
- α-Klotho prevents diabetic retinopathy by reversing the senescence of macrophages.Cell communication and signaling : CCS · 2024Article
- Adipose Tissue Dysfunction and the Role of Adipocyte-Derived Extracellular Vesicles in Obesity and Metabolic Syndrome.Journal of the Endocrine Society · 2024Review
- Glucosamine substituted sulfonylureas: IRS-PI3K-PKC-AKT-GLUT4 insulin signalling pathway intriguing agent.RSC medicinal chemistry · 2024Article
- Green Synthesis and Characterization of Silver Nanoparticles UsingPharmaceuticals (Basel, Switzerland) · 2023Article
- Is Insulin Receptor Substrate4 (IRS4) a Platform Involved in the Activation of Several Oncogenes?Cancers · 2023Review
- The effect of hormones insulin and glucagon on ubiquitin modifications elucidated by proteomics in liver cells.Life sciences · 2023Article
- DLBS3233 enhances nephrin and podocin expression also reduces oxidative stress marker and insulin receptor serine diabetic rats' podocytes.Annals of medicine and surgery (2012) · 2023Article
- VAPB-mediated ER-targeting stabilizes IRS-1 signalosomes to regulate insulin/IGF signaling.Cell discovery · 2023Article
- Decoding of miR-7-5p in Colony Forming Unit-Hill Colonies as a Biomarker of Subclinical Cardiovascular Disease-A MERIT Study.International journal of molecular sciences · 2023Article
- Molecular Mechanisms for the Vicious Cycle between Insulin Resistance and the Inflammatory Response in Obesity.International journal of molecular sciences · 2023Review
- Management of diabesity: Current concepts.World journal of diabetes · 2023Review
- PMFrontiers in endocrinology · 2023Article
- The Role of Insulin Receptor Substrate Proteins in Bronchopulmonary Dysplasia and Asthma: New Potential Perspectives.International journal of molecular sciences · 2022Review
- Article
- Metformin and Gegen Qinlian Decoction boost islet α-cell proliferation of the STZ induced diabetic rats.BMC complementary medicine and therapies · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
IRS proteins are cellular adaptor molecules that mediate many of the key metabolic actions of insulin. When tyrosine is phosphorylated by the activated insulin receptor, IRS proteins recruit downstream effectors, such as phosphoinositide 3-kinase and mitogen-activated protein kinase, in order to elicit cellular responses such as glucose uptake, lipid metabolism and cell proliferation. There are two main IRS proteins in humans (IRS1 and IRS2), both of which are widely expressed. Given their central role in the insulin signalling pathway, it is not surprising that male mice lacking Irs1 or Irs2 present with elevated blood glucose or type 2 diabetes, respectively. For reasons yet to be identified, female Irs2 (-/-) mice do not develop type 2 diabetes. A number of organs are affected by complications of diabetes; macrovascular complications include stroke and coronary artery disease, while nephropathy, neuropathy and retinopathy fall into the category of microvascular complications. Given the serious consequences of these complications on patient morbidity and mortality, it is essential to identify the molecular pathogenesis underlying diabetic complications, with a view to improving therapeutic intervention and patient outcomes. A number of recently published papers have converged on the hypothesis that the loss of insulin signalling and IRS proteins is instrumental to the development and/or progression of diabetic complications. This review will summarise some highlights from the published work in which this hypothesis is discussed.
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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.