ArticleInternational journal of molecular medicine2019
Erythropoietin suppresses hepatic steatosis and obesity by inhibiting endoplasmic reticulum stress and upregulating fibroblast growth factor 21.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 14 citations in OpenAlex.
- Gut‑liver‑kidney axis: A systems biology framework for understanding and treating chronic kidney disease (Review).International journal of molecular medicine · 2026Review
- Tranexamic acid and erythropoietin inhibited inflammatory response and endoplasmic reticulum stress and protected rats against acute lung injury caused by osteoporotic hip fracture.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2025Article
- Fine Particulate Matter (Environmental health perspectives · 2025Article
- Research progress on endoplasmic reticulum homeostasis in acute kidney injury.Frontiers in pharmacology · 2025Review
- Severe Hyporesponsiveness to Erythropoiesis-Stimulating Agents in Patients on Chronic Hemodialysis-Reconsidering the Relationship with Thrombo-Inflammation and Oxidative Stress.Diagnostics (Basel, Switzerland) · 2024Article
- Mechanism of Action and Related Natural Regulators of Nrf2 in Nonalcoholic Fatty Liver Disease.Current drug delivery · 2024Review
- SIRT1 is transcriptionally repressed by YY1 and suppresses ferroptosis in rheumatoid arthritis.Advances in rheumatology (London, England) · 2023Article
- Endoplasmic reticulum stress-mediated cell death in liver injury.Cell death & disease · 2022Review
- Differentiating between liver diseases by applying multiclass machine learning approaches to transcriptomics of liver tissue or blood-based samples.JHEP reports : innovation in hepatology · 2022Article
- Erythropoietin regulates metabolic response in mice via receptor expression in adipose tissue, brain, and bone.Experimental hematology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Erythropoietin (EPO), known primarily for its role in erythropoiesis, was recently reported to play a beneficial role in regulating lipid metabolism; however, the underlying mechanism through which EPO decreases hepatic lipid accumulation requires further investigation. Endoplasmic reticulum (ER) stress may contribute to the progression of hepatic steatosis. The present study investigated the effects of EPO on regulating ER stress in fatty liver. It was demonstrated that EPO inhibited hepatic ER stress and steatosis in vivo and in vitro. Interestingly, these beneficial effects were abrogated in liver‑specific sirtuin 1 (SIRT1)‑knockout mice compared with wild‑type littermates. In addition, in palmitate‑treated hepatocytes, small interfering RNA‑mediated SIRT1 silencing suppressed the effects of EPO on lipid‑induced ER stress. Additionally, EPO stimulated hepatic fibroblast growth factor 21 (FGF21) expression and secretion in a SIRT1‑dependent manner in mice. Furthermore, the sensitivity of hepatocytes from obese mice to FGF21 was restored following treatment with EPO. Collectively, the results of the present study revealed a new mechanism underlying the regulation of hepatic ER stress and FGF21 expression induced by EPO; thus, EPO may be considered as a potential therapeutic agent for the treatment of fatty liver and obesity.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.