ArticleBritish journal of pharmacology2015
Prolyl hydroxylase inhibition corrects functional iron deficiency and inflammation-induced anaemia in rats.
Article in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.
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Who cites it
20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.
- UK kidney association clinical practice guideline: update of anaemia of chronic kidney disease.BMC nephrology · 2025Guideline
- Effects of hypoxia-inducible factor-prolyl hydroxylase inhibitorsFrontiers in endocrinology · 2023Pooled it
- An Almond Meal-Rich Diet Improves Red Blood Cell Count and Reduces Odds of Anemia in a Mouse Model of Aging.Antioxidants (Basel, Switzerland) · 2026Article
- Article
- The Inflammatory Milieu Exacerbates Anemia of Chronic Kidney Disease: From the Gut-Kidney Axis to Bone Marrow Hematopoiesis Inhibition.Kidney & blood pressure research · 2026Review
- The Azalea Hypothesis of Alzheimer Disease: A Functional Iron Deficiency Promotes Neurodegeneration.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- Review
- Hypoxia-Inducible Factor-Prolyl Hydroxylase Inhibitor Improves Leukocyte Energy Metabolism in Hereditary Hemorrhagic Telangiectasia.Life (Basel, Switzerland) · 2023Article
- EPO synthesis induced by HIF-PHD inhibition is dependent on myofibroblast transdifferentiation and colocalizes with non-injured nephron segments in murine kidney fibrosis.Acta physiologica (Oxford, England) · 2022Article
- The Role of Iron in Benign and Malignant Hematopoiesis.Antioxidants & redox signaling · 2021Review
- Hypoxia-inducible factor-prolyl hydroxylase inhibitors in the treatment of anemia of chronic kidney disease.Kidney international supplements · 2021Article
- Article
- Understanding the Oxygen-Sensing Pathway and Its Therapeutic Implications in Diseases.The American journal of pathology · 2020Review
- Hypoxia-Inducible Factor Activators in Renal Anemia: Current Clinical Experience.Advances in chronic kidney disease · 2019Review
- Article
- The interplay between iron and oxygen homeostasis with a particular focus on the heart.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Review
- Therapeutic targeting of the HIF oxygen-sensing pathway: Lessons learned from clinical studies.Experimental cell research · 2017Review
- Targeting iron metabolism in drug discovery and delivery.Nature reviews. Drug discovery · 2017Review
- HIF-prolyl hydroxylases as therapeutic targets in erythropoiesis and iron metabolism.Hemodialysis international. International Symposium on Home Hemodialysis · 2017Review
- Hypoxia Induced Factor in Chronic Kidney Disease: Friend or Foe?Frontiers in medicine · 2017Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeSmall-molecule inhibitors of prolyl hydroxylase (PHD) enzymes are a novel target for the treatment of anaemia and functional iron deficiency (FID). Other than being orally bioavailable, the differentiation of PHD inhibitors from recombinant human erythropoietin (rhEPO) has not been demonstrated. EXPERIMENTAL APPROACH: JNJ-42905343 was identified and characterized as a novel inhibitor of PHD and its action was compared with rhEPO in healthy rats and in a rat model of inflammation-induced anaemia and FID [peptidoglycan-polysaccharide (PGPS) model]. KEY
resultsOral administration of JNJ-42905343 to healthy rats increased the gene expression of cytochrome b (DcytB) and divalent metal-ion transporter 1 (DMT1) in the duodenum, and increased plasma EPO. Repeated administration of JNJ-42905343 for 28 days increased blood haemoglobin, mean corpuscular haemoglobin (MCH) and mean corpuscular volume (MCV). The serum iron concentration was increased with low doses (0.3 mg·kg(-1) ) but reduced at high doses (6 mg·kg(-1) ). In PGPS-treated rats, administration of JNJ-42905343 for 28 days corrected FID and anaemia, as reflected by increased blood haemoglobin, MCH and MCV. Increased expression of DcytB and DMT1 genes in the duodenum resulting in increased iron availability was defined as the mechanism for these effects. rhEPO did not affect DcytB and DMT1 and was not effective in PGPS-treated rats. CONCLUSIONS AND IMPLICATIONS: PHD inhibition has a beneficial effect on iron metabolism in addition to stimulating the release of EPO. Small-molecule inhibitors of PHD such as JNJ-42905343 represent a mechanism distinct from rhEPO to treat anaemia and FID.
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