ArticleProceedings of the National Academy of Sciences of the United States of America2021
Agonist of growth hormone-releasing hormone enhances retinal ganglion cell protection induced by macrophages after optic nerve injury.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. 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, 19 citations in OpenAlex.
- Growth hormone-releasing hormone attenuates amyloid deposition and neuroinflammation in Alzheimer's disease models.Cell death & disease · 2026Article
- GHRHR Deficiency Enhances Retinal Ganglion Cell Survival and Visual Functions in Experimental Glaucoma by Inhibiting Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Role of Growth Hormone (GH) and Other Somatotropic Axis Elements in Retinal Neuroprotection.Current issues in molecular biology · 2026Review
- Dose-optimized HILT promotes peripheral nerve repair through BMP4-Smad9-mediated inhibition of neuroinflammation and oxidative stress.APL bioengineering · 2026Article
- Growth hormone-releasing hormone in retinal disorders and uveitis: an updated review.International journal of ophthalmology · 2026Review
- The development of growth hormone-releasing hormone analogs: Therapeutic advances in cancer, regenerative medicine, and metabolic disorders.Reviews in endocrine & metabolic disorders · 2025Review
- Effects of GHRH and its analogues on the Vascular System.Reviews in endocrine & metabolic disorders · 2025Review
- Evaluating the Evidence for Neuroprotective and Axonal Regenerative Activities of Different Inflammatory Cell Types After Optic Nerve Injury.Molecular neurobiology · 2025Review
- Growth hormone-releasing hormone and its analogues in health and disease.Nature reviews. Endocrinology · 2025Review
- The IL-33/ST2 Axis Protects Retinal Ganglion Cells by Modulating the Astrocyte Response After Optic Nerve Injury.Neuroscience bulletin · 2025Article
- Cellular senescence mediates retinal ganglion cell survival regulation post-optic nerve crush injury.Cell proliferation · 2024Article
- Growth Hormone Neuroprotective Effects After an Optic Nerve Crush in the Male Rat.Investigative ophthalmology & visual science · 2024Article
- Growth hormone releasing hormone signaling promotes Th17 cell differentiation and autoimmune inflammation.Nature communications · 2023Article
- Growth hormone-releasing hormone receptor signaling in experimental ocular inflammation and neuroprotection.Neural regeneration research · 2022Review
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Optic neuropathies are leading causes of irreversible visual impairment and blindness, currently affecting more than 100 million people worldwide. Glaucoma is a group of optic neuropathies attributed to progressive degeneration of retinal ganglion cells (RGCs). We have previously demonstrated an increase in survival of RGCs by the activation of macrophages, whereas the inhibition of macrophages was involved in the alleviation on endotoxin-induced inflammation by antagonist of growth hormone-releasing hormone (GHRH). Herein, we hypothesized that GHRH receptor (GHRH-R) signaling could be involved in the survival of RGCs mediated by inflammation. We found the expression of GHRH-R in RGCs of adult rat retina. After optic nerve crush, subcutaneous application of GHRH agonist MR-409 or antagonist MIA-602 promoted the survival of RGCs. Both the GHRH agonist and antagonist increased the phosphorylation of Akt in the retina, but only agonist MR-409 promoted microglia activation in the retina. The antagonist MIA-602 reduced significantly the expression of inflammation-related genes
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Registered trials
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