ReviewNeurochemical research2012
Role of oxidative stress and Ca²⁺ signaling on molecular pathways of neuropathic pain in diabetes: focus on TRP channels.
Review in Neurochemical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 139 citations in OpenAlex.
- Review
- Selenium reduces oxaliplatin induced neuropathic pain: focus on TRPV1.Frontiers in pharmacology · 2025Article
- Association of Plasma Metal Levels with Outcomes of Assisted Reproduction in Polycystic Ovary Syndrome.Biological trace element research · 2024Article
- Resveratrol Modulates Diabetes-Induced Neuropathic Pain, Apoptosis, and Oxidative Neurotoxicity in Mice Through TRPV4 Channel Inhibition.Molecular neurobiology · 2024Article
- Omega 3 fatty acids preserve testicular function by ameliorating BPF-induced dysthyroidism: role of p53/Bcl-2 signaling and proton pump activities.JBRA assisted reproduction · 2024Article
- Single-fiber probes for combined sensing and imaging in biological tissue: recent developments and prospects.Biomedical optics express · 2024Review
- High-throughput screening of transient receptor potential (TRP) channels in pterygium.International ophthalmology · 2024Article
- Involvement of Oxidative Stress and Nutrition in the Anatomy of Orofacial Pain.International journal of molecular sciences · 2023Review
- Selenium Protects ARPE-19 and ACBRI 181 Cells against High Glucose-Induced Oxidative Stress.Molecules (Basel, Switzerland) · 2023Article
- Involvement of TRPM7 Channel on the Induction of Diabetic Neuropathic Pain in Mice: Protective Role of Selenium and Curcumin.Biological trace element research · 2023Article
- Dietary phytate induces subclinical mechanical allodynia in mice.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023Article
- Carvacrol protects the ARPE19 retinal pigment epithelial cells against high glucose-induced oxidative stress, apoptosis, and inflammation by suppressing the TRPM2 channel signaling pathways.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022Article
- A novel antagonist of TRPM2 and TRPV4 channels: Carvacrol.Metabolic brain disease · 2022Article
- Noopept Attenuates Diabetes-Mediated Neuropathic Pain and Oxidative Hippocampal Neurotoxicity via Inhibition of TRPV1 Channel in Rats.Molecular neurobiology · 2021Article
- Curcumin Attenuates Hypoxia-Induced Oxidative Neurotoxicity, Apoptosis, Calcium, and Zinc Ion Influxes in a Neuronal Cell Line: Involvement of TRPM2 Channel.Neurotoxicity research · 2021Article
- 7β-(3-Ethyl-Molecules (Basel, Switzerland) · 2021Article
- Transcriptome Analysis Reveals the Role of Cellular Calcium Disorder in Varicella Zoster Virus-Induced Post-Herpetic Neuralgia.Frontiers in molecular neuroscience · 2021Article
- Unsupervised clustering of multiparametric fluorescent images extends the spectrum of detectable cell membrane phases with sub-micrometric resolution.Biomedical optics express · 2020Article
- FEATURE SELECTION FOR GENERALIZED VARYING COEFFICIENT MIXED-EFFECT MODELS WITH APPLICATION TO OBESITY GWAS.The annals of applied statistics · 2020Article
- Hydroethanolic Stem Bark Extract ofAdvances in pharmacological and pharmaceutical sciences · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes mellitus, a debilitating chronic disease, affects ~100 million people. Peripheral neuropathy is one of the most common early complications of diabetes in ~66 % of these patients. Altered Ca(2+) handling and Ca(2+) signaling were detected in a huge variety of preparations isolated from animals with experimentally induced type 1 and 2 diabetes as well as patients suffering from the disease. We reviewed the role of Ca(2+) signaling through cation channels and oxidative stress on diabetic neuropathic pain in sensory neurons. The pathogenesis of diabetic neuropathy involves the polyol pathway, advanced glycation end products, oxidative stress, protein kinase C activation, neurotrophism, and hypoxia. Experimental studies with respect to oxidative stress and Ca(2+) signaling, inhibitor roles of antioxidants in diabetic neuropathic pain are also summarized in the review. We hypothesize that deficits in insulin, triggers alterations of sensory neurone phenotype that are critical for the development of abnormal Ca(2+) homeostasis and oxidative stress and associated mitochondrial dysfunction. The transient receptor potential channels are a large family of proteins with six main subfamilies. The sheer number of different TRPs with distinct functions supports the statement that these channels are involved in a wide range of processes ranging in diabetic neuropathic pain and it seems that the TRPC, TRPM and TRPV groups are mostly responsible from diabetic neuropathic pain. In conclusion, the accumulating evidence implicating Ca(2+) dysregulation and over production of oxidative stress products in diabetic neuropathic pains, along with recent advances in understanding of genetic variations in cation channels such as TRP channels, makes modulation of neuronal Ca(2+) handling an increasingly viable approach for therapeutic interventions against the painful and degenerative aspects of many diabetic neuropathies.
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