ArticleBioengineered2022
Carvedilol activates nuclear factor E2-related factor 2/ antioxidant response element pathway to inhibit oxidative stress and apoptosis of retinal pigment epithelial cells induced by high glucose.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Protective Effect of Carvedilol Against Oxidative Stress Induced by Palmitic Acid in Primary Rat Hepatocytes.Cell biochemistry and function · 2025Article
- Impact of early β-blocker use on the incidence of sepsis and clinical outcomes following cardiac surgery: a retrospective cohort study.Frontiers in pharmacology · 2025Article
- Carvedilol Confers Ferroptosis Resistance in HL-1 Cells by Upregulating GPX4, FTH1, and FTL1 and Inducing Metabolic Remodeling Under Hypoxia/Reoxygenation.Antioxidants (Basel, Switzerland) · 2024Article
- Deletion of Nrf2 induced severe oxidative stress and apoptosis in mice model of diabetic bladder dysfunction.International urology and nephrology · 2024Article
- Linoleic Acid Alleviates Lipopolysaccharide Induced Acute Liver Injury via Activation of Nrf2.Physiological research · 2024Article
- Heyingwuzi formulation alleviates diabetic retinopathy by promoting mitophagyWorld journal of diabetes · 2024Article
- Biomarker evidence of early vision and rod energy-linked pathophysiology benefits from very low dose DMSO in 5xFAD mice.Acta neuropathologica communications · 2024Article
- β-blockers and metabolic modulation: unraveling the complex interplay with glucose metabolism, inflammation and oxidative stress.Frontiers in pharmacology · 2024Review
- Diabetic Cardiomyopathy Uncovered: Transcriptomics, NLRP3, and Carvedilol Mechanisms.Journal of diabetes research · 2024Article
- Alleviate oxidative stress in diabetic retinopathy: antioxidant therapeutic strategies.Redox report : communications in free radical research · 2023Review
- Recombinant human klotho protects against hydrogen peroxide-mediated injury in human retinal pigment epithelial cells via the PI3K/Akt-Nrf2/HO-1 signaling pathway.Bioengineered · 2022Article
- MiR-192 attenuates high glucose-induced pyroptosis in retinal pigment epithelial cells via inflammasome modulation.Bioengineered · 2022Article
- Oncogenic Forkhead box D3 antisense RNA 1 promotes cell survival and confers temozolomide resistance in glioblastoma cells through the miR-128-3p/WEE1 G2 checkpoint kinase axis.Bioengineered · 2022Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic retinopathy (DR) is the most prominent manifestation of diabetic microangiopathy and is a serious complication of diabetes. Despite extensive researches focusing on DR, treatment options for DR are still limited. Carvedilol (CAR) has vasodilatory, antioxidant stress and anti-inflammatory effects and poses a vital role in addressing the issue of diabetic complications. This paper attempts to explore this property of CAR and investigate into its effects on DR. First, ARPE-19 cells were treated with different concentrations of CAR and cells were induced with 30 mM high glucose (HG) to establish a DR cell model. Cell viability was assayed by cell counting kit-8 (CCK-8) with or without HG induction. Cellular inflammation and oxidative stress were evaluated by enzyme-linked immunosorbent assay (ELISA) and corresponding kits. The measurement of apoptosis levels was conducted by Terminal dUTP nick-end labeling (TUNEL) and Western blotting. The protein levels related to Nrf2/ARE signaling pathway were assessed by Western blotting. Finally, cellular inflammation, oxidative stress and apoptosis in ARPE-19 cells pretreated with Nrf2 inhibitor ML385 were tested again by the same methods. Results showed that under HG induction, CAR effectively improved ARPE-19 cell viability, inhibited cellular inflammation, oxidative stress, and apoptosis. Moreover, CAR activated Nrf2/ARE signaling pathway, which further suppressed cellular inflammation, oxidative stress, and apoptosis. Overall, CAR inhibited HG-induced oxidative stress and apoptosis in retinal pigment epithelial cells by activating Nrf2/ARE pathway.
Indexed as
Identifiers
What Socratic holds
Registered trials
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 Socratic graph.