ArticleOxidative medicine and cellular longevity2021
TSH Combined with TSHR Aggravates Diabetic Peripheral Neuropathy by Promoting Oxidative Stress and Apoptosis in Schwann Cells.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Exercise Training Regulates Cortical GPCR-Mediated Signaling Networks Through cAMP, Calcium, and Neuroactive Ligand-Receptor Interaction Pathways in Diabetic-Obese Rats: An In Silico Study.International journal of molecular sciences · 2026Article
- Analysis of correlated factors of skin pruritus in type 2 diabetes mellitus.BMC endocrine disorders · 2026Observational
- The role of clinical laboratory parameters in diabetic neuropathy: correlations and recent advances.Frontiers in endocrinology · 2026Review
- Protein S-acylation: Pathological mechanisms and novel therapeutic targets for diabetic complications.Chinese herbal medicines · 2026Review
- Antihypertensive Drug Amlodipine Besylate Shows Potential in Alleviating Diabetic Peripheral Neuropathy.Diabetes · 2025Article
- Natural therapy proposed for the management of diabetic peripheral neuropathy (DPN).Inflammopharmacology · 2025Review
- Differential Impact of Metabolic Factors and Comorbidities on Peripheral Neuropathy.Journal of the peripheral nervous system : JPNS · 2025Article
- Targeting oxidative damage in diabetic foot ulcers: integrative strategies involving antioxidant drugs and nanotechnologies.Burns & trauma · 2025Review
- Elevated thyroid-stimulating hormone correlates with insulin resistance and β-cell dysfunction in type 2 diabetes with subclinical hypothyroidism.American journal of translational research · 2025Article
- Wheat grain moxibustion ameliorates oxidative stress in PTU-induced hypothyroid rats via cAMP/PKA pathway activation.Frontiers in endocrinology · 2025Article
- Increased thyroid stimulating hormone (TSH) as a possible risk factor for atherosclerosis in subclinical hypothyroidism.Thyroid research · 2024Review
- Impaired autonomic function and somatosensory disturbance in patients with treated autoimmune thyroiditis.Scientific reports · 2024Article
- Review
- Diabetic peripheral neuropathy: pathogenetic mechanisms and treatment.Frontiers in endocrinology · 2023Review
- Serum Uric Acid Levels Are Related to Diabetic Peripheral Neuropathy, Especially for Motor Conduction Velocity of Tibial Nerve in Type 2 Diabetes Mellitus Patients.Journal of diabetes research · 2023Article
- Hypothyroidism and Diabetes-Related Dementia: Focused on Neuronal Dysfunction, Insulin Resistance, and Dyslipidemia.International journal of molecular sciences · 2022Review
- Correlation of thyroid-related hormones with vascular complications in type 2 diabetes patients with euthyroid.Frontiers in endocrinology · 2022Article
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Authors and funding
6 authors.
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Abstract
Subclinical hypothyroidism (SCH) is associated with diabetic peripheral neuropathy (DPN); however, the mechanism underlying this association remains unknown. This study is aimed at examining neurofunctional and histopathological alterations in a type 2 diabetes (T2DM) mouse model of SCH and investigating the impact of thyroid-stimulating hormone (TSH) in an in vitro DPN cell model established using RSC96 cells under high glucose (HG) and palmitic acid (PA) stimulation. Our results indicated that T2DM, in combination with SCH, aggravated abnormal glucose and lipid metabolism in T2DM and dramatically destroyed the peripheral nervous system by increasing paw withdrawal latency, decreasing motor nerve conduction velocity, and exacerbating ultrastructural deterioration of the damaged sciatic nerve caused by diabetes. Furthermore, the results of our in vitro experiments showed that TSH intensified HG/PA-induced RSC96 cell damage by inducing oxidative stress, mitochondrial dysfunction, and apoptosis. More importantly, TSHR knockout or inhibition of PA-induced TSHR palmitoylation could alleviate the apoptosis induced by TSH. Overall, in this study, the novel mechanisms by which TSH, as an independent risk factor for DPN progression, aggravating Schwann cell apoptosis and demyelination, are elucidated. These findings indicate that TSHR could be a potential target for both the prevention and treatment of DPN and, possibly, other microvascular diseases, and have implication in the clinical management of patients with DPN.
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