ArticleJCI insight2022
Loss of TRPV2-mediated blood flow autoregulation recapitulates diabetic retinopathy in rats.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Circular RNA circPSEN1 promotes neovascularization by regulating the miR-150-5p/TRIM65 axis in diabetic retinopathy.Biochemistry and biophysics reports · 2026Article
- The association between lower extremity physical performance and diabetic retinopathy among patients with type 2 diabetes in Shaoguan City, China.BMC ophthalmology · 2026Article
- Retinal Microvascular Resistance Estimated From Waveform Analysis Is Significantly Higher in Diabetic Retinopathy.Translational vision science & technology · 2025Article
- Scavenging acrolein with 2-HDP preserves neurovascular integrity in a rat model of diabetic retinal disease.Diabetologia · 2025Article
- The Calcium Signalling Profile of the Inner Blood-Retinal Barrier in Diabetic Retinopathy.Cells · 2025Review
- Sitagliptin eye drops prevent the impairment of retinal neurovascular unit in the new Trpv2Journal of neuroinflammation · 2024Article
- Activation of BK channels prevents diabetes-induced osteopenia by regulating mitochondrial CaAutophagy · 2024Article
- Role of transient receptor potential channels in the regulation of vascular tone.Drug discovery today · 2024Review
- The Variety of Mechanosensitive Ion Channels in Retinal Neurons.International journal of molecular sciences · 2024Review
- Transient Receptor Potential Channels in the Healthy and Diseased Blood-Brain Barrier.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024Review
- Relation Between Reactive Oxygen Species Production and Transient Receptor Potential Vanilloid1 Expression in Human Skin During Aging.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024Article
- Impact of aging on vascular ion channels: perspectives and knowledge gaps across major organ systems.American journal of physiology. Heart and circulatory physiology · 2023Review
- IL-33 regulates Müller cell-mediated retinal inflammation and neurodegeneration in diabetic retinopathy.Disease models & mechanisms · 2023Article
- Retinal Ischaemia in Diabetic Retinopathy: Understanding and Overcoming a Therapeutic Challenge.Journal of clinical medicine · 2023Review
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Authors and funding
19 authors at 1 institution in 1 country.
Funding
Abstract
Loss of retinal blood flow autoregulation is an early feature of diabetes that precedes the development of clinically recognizable diabetic retinopathy (DR). Retinal blood flow autoregulation is mediated by the myogenic response of the retinal arterial vessels, a process that is initiated by the stretch‑dependent activation of TRPV2 channels on the retinal vascular smooth muscle cells (VSMCs). Here, we show that the impaired myogenic reaction of retinal arterioles from diabetic animals is associated with a complete loss of stretch‑dependent TRPV2 current activity on the retinal VSMCs. This effect could be attributed, in part, to TRPV2 channel downregulation, a phenomenon that was also evident in human retinal VSMCs from diabetic donors. We also demonstrate that TRPV2 heterozygous rats, a nondiabetic model of impaired myogenic reactivity and blood flow autoregulation in the retina, develop a range of microvascular, glial, and neuronal lesions resembling those observed in DR, including neovascular complexes. No overt kidney pathology was observed in these animals. Our data suggest that TRPV2 dysfunction underlies the loss of retinal blood flow autoregulation in diabetes and provide strong support for the hypothesis that autoregulatory deficits are involved in the pathogenesis of DR.
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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.