ArticleJournal of diabetes research2020
Function of Adenosine 2A Receptor in High-Fat Diet-Induced Peripheral Neuropathy.
Article in Journal of diabetes research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed, 4 citations in OpenAlex.
- The underexplored role of neuropilins in chronic pain pathophysiology: a review.Molecular biology reports · 2026Review
- Keratinocyte-Derived Exosomes in Painful Diabetic Neuropathy.bioRxiv : the preprint server for biology · 2024Article
- Keratinocyte-derived extracellular vesicles in painful diabetic neuropathy.Neurobiology of pain (Cambridge, Mass.)Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peripheral diabetic neuropathy (DPN) is a complication observed in up to half of all patients with type 2 diabetes. DPN has also been shown to be associated with obesity. High-fat diet (HFD) affects glucose metabolism, and the impaired glucose tolerance can lead to type 2 diabetes. There is evidence to suggest a role of adenosine 2A receptors (A2ARs) and semaphorin 3A (Sema3a) signaling in DPN. The link between the expression of Sema3a and A2AR in DPN was hypothesized, but the underlying mechanisms remain poorly understood. In this study, we investigated the regulation of Sema3a by A2AR in the spinal cord and the functional implications thereof in DPN. We examined the expression of A2ARs and Sema3a, as well as Neuropilin 1 and Plexin A, the coreceptors of Sema3a, in the dorsal horn of the lumbar spinal cord of an animal model with HFD-induced diabetes. Our results demonstrate that HFD dysregulates the A2AR-mediated Sema3a expression, with functional implications for the type 2 diabetes-induced peripheral neuropathy. These observations could stimulate clinical studies to improve our understanding on the subject.
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