ReviewCell stress & chaperones2023
Nutri-stress, mitochondrial dysfunction, and insulin resistance-role of heat shock proteins.
Review in Cell stress & chaperones, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Extracellular vesicles participate in proteostasis and heat shock adaptation inEmerging microbes & infections · 2026Article
- Heat Shock Proteins and Exercise in Skeletal Muscle Insulin Resistance: Protective Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2026Review
- Metainflammation, Mitochondrial Dysfunction, and Organokine Crosstalk: A Central Axis Linking Metabolic Syndrome to Cardiovascular Diseases.International journal of molecular sciences · 2026Review
- Mechanisms of Heat-Induced Sleep Disruption in Aging: A Narrative Review.Clocks & sleep · 2026Review
- Sociodemographic, Lifestyle, and Social Isolation Correlates of TyG, METS-IR, and SPISE-IR Scores in a Large Spanish Working Population.Medical sciences (Basel, Switzerland) · 2025Article
- Heat shock proteins in hypothermia: a review.Frontiers in molecular biosciences · 2025Review
- Pancreatic Antioxidative Defense and Heat Shock Proteins Prevent Islet of Langerhans Cell Death After Chronic Oral Exposure to Cadmium LOAEL Dose.Biological trace element research · 2024Article
- Article
- [Analysis of Risk Factors for Recurrent Pregnancy Loss in Patients UndergoingSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024Article
- Impact of Polyethylene Terephthalate Microplastics onBiology · 2024Article
- Review
- Thermal Effect on Heat Shock Protein 70 Family to Prevent Atherosclerotic Cardiovascular Disease.Biomolecules · 2023Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excess nutrient flux into the cellular energy system results in a scenario of cellular metabolic stress in diseases involving insulin resistance, such as type 2 diabetes, referred to as nutri-stress and results in cellular bioenergetic imbalance, which leads to insulin resistance and disease. Under nutri-stress, the heat shock response system is compromised due to metabolic abnormalities that disturb energy homeostasis. Heat shock proteins (HSPs) are the chief protectors of intracellular homeostasis during stress. Heat shock response (HSR) impairment contributes to several metabolic pathways that aggravate chronic hyperglycaemia and insulin resistance, highlighting a central role in disease pathogenesis. This article discusses the role of nutri-stress-related molecular events in causing insulin resistance and the nature of the roles played by heat shock proteins in some of the crucial checkpoints of the molecular networks involved in insulin resistance. Ample evidence suggests that the heat shock machinery regulates critical pathways in mitochondrial function and energy metabolism and that cellular energy status highly influences it. Weakening of HSPs, therefore, leads to loss of their vital cytoprotective functions, propagating nutri-stress in the system. Further research into the mechanistic roles of HSPs in metabolic homeostasis will help widen our understanding of lifestyle diseases, their onset, and complications. These inducible proteins may be crucial to attenuating lifestyle risk factors and disease management.
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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.