Special Issue "Advances in Iron Deficiency and Iron-Related Disorders"

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Endocrinology and Metabolism Research".

Deadline for manuscript submissions: 31 January 2024 | Viewed by 1900

Special Issue Editor

Department of Clinical Biochemistry, Oxford University Hospitals, Oxford OX3 9DU, UK
Interests: biomarkers; mitochondrial diseases; dementia; iron pathophysiology; liver allograft function

Special Issue Information

Dear Colleagues,

Iron status influences a vast array of cellular processes.  Iron imbalance or dysregulation can have adverse, clinically-significant  effects on gene regulation, enzyme activities, mitochondrial function, stress response and even cell viability.  Absolute or functional iron deficiency can lead to morbidity, impairs neurobehavioural development in early life, predisposes to immune dysfunction, and is associated with adverse outcomes in patients with cancer, heart failure or those undergoing surgery.  At the other end of the spectrum, iron has been associated with inflammatory processes, oxidative stress, mitochondrial dysfunction and ferroptosis.  Some of these and related cellular events have implications for neurodegenerative, cardiovascular, pulmonary, hepatic and other disorders.  The expanding knowledge of the involvement of iron in cellular function has encouraged exciting avenues of research that are increasing our understanding of the pathogenic mechanisms of some common diseases, and may pave the way for interventions that would alleviate those conditions or improve clinical outcomes.

It gives me great pleasure to invite researchers who are studying cellular processes and mechanisms of disease in which iron plays a significant role to submit their original research or review papers for this special issue of Biomedicines.  The aim of this special issue is to offer emerging knowledge or overviews of the pathophysiological mechanisms through which iron imbalance may bring about clinical effects.  Research involving clinical studies or the use of human cells are especially, but not exclusively, welcome.

Dr. Alireza Morovat
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • iron deficiency
  • iron overload
  • pathophysiology
  • inflammation
  • organ disorders
  • cancer
  • neurodegenerative disease
  • immune function
  • therapy

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

14 pages, 1276 KiB  
Article
Factors Governing the Erythropoietic Response to Intravenous Iron Infusion in Patients with Chronic Kidney Disease: A Retrospective Cohort Study
Biomedicines 2023, 11(9), 2417; https://doi.org/10.3390/biomedicines11092417 - 29 Aug 2023
Viewed by 598
Abstract
Background: Limited knowledge exists about factors affecting parenteral iron response. A study was conducted to determine the factors influencing the erythropoietic response to parenteral iron in iron-deficient anaemic patients whose kidney function ranged from normal through all stages of chronic kidney disease (CKD) [...] Read more.
Background: Limited knowledge exists about factors affecting parenteral iron response. A study was conducted to determine the factors influencing the erythropoietic response to parenteral iron in iron-deficient anaemic patients whose kidney function ranged from normal through all stages of chronic kidney disease (CKD) severity. Methods: This retrospective cohort study included parenteral iron recipients who did not receive erythropoiesis-stimulating agents (ESA) between 2017 and 2019. The study cohort was derived from two groups of patients: those managed by the CKD team and patients being optimised for surgery in the pre-operative clinic. Patients were categorized based on their kidney function: Patients with normal kidney function [estimated glomerular filtration rate (eGFR) ≥ 60 mL/min/1.73 m2] were compared to those with CKD stages 3–5 (eGFR < 60 mL/min/1.73 m2). Patients were further stratified by the type of iron deficiency [absolute iron deficiency (AID) versus functional iron deficiency (FID)]. The key outcome was change in hemoglobin (∆Hb) between pre- and post-infusion haemoglobin (Hb) values. Parenteral iron response was assessed using propensity-score matching and multivariate linear regression. The impact of kidney impairment versus the nature of iron deficiency (AID vs. FID) in response was explored. Results: 732 subjects (mean age 66 ± 17 years, 56% females and 87% White) were evaluated. No significant differences were observed in the time to repeat Hb among CKD stages and FID/AID patients. The Hb rise was significantly lower with lower kidney function (non-CKD and CKD1–2; 13 g/L, CKD3–5; 7 g/L; p < 0.001). When groups with different degrees of renal impairment were propensity-score matched according to whether iron deficiency was due to AID or FID, the level of CKD was found not to be relevant to Hb responses [unmatched (∆Hb) 12.1 vs. 8.7 g/L; matched (∆Hb) 12.4 vs. 12.1 g/L in non-CKD and CKD1–2 versus CKD3–5, respectively]. However, a comparison of patients with AID and FID, while controlling for the degree of CKD, indicated that patients with FID exhibited a diminished Hb response regardless of their level of kidney impairment. Conclusion: The nature of iron deficiency rather than the severity of CKD has a stronger impact on Hb response to intravenous iron with an attenuated response seen in functional iron deficiency irrespective of the degree of renal impairment. Full article
(This article belongs to the Special Issue Advances in Iron Deficiency and Iron-Related Disorders)
Show Figures

Graphical abstract

15 pages, 5731 KiB  
Article
High Hepcidin Levels Promote Abnormal Iron Metabolism and Ferroptosis in Chronic Atrophic Gastritis
Biomedicines 2023, 11(9), 2338; https://doi.org/10.3390/biomedicines11092338 - 22 Aug 2023
Viewed by 691
Abstract
Background: Chronic atrophic gastritis (CAG) is a chronic inflammatory disease and premalignant lesion of gastric cancer. As an antimicrobial peptide, hepcidin can maintain iron metabolic balance and is susceptible to inflammation. Objectives: The objective of this study was to clarify whether hepcidin is [...] Read more.
Background: Chronic atrophic gastritis (CAG) is a chronic inflammatory disease and premalignant lesion of gastric cancer. As an antimicrobial peptide, hepcidin can maintain iron metabolic balance and is susceptible to inflammation. Objectives: The objective of this study was to clarify whether hepcidin is involved in abnormal iron metabolism and ferroptosis during CAG pathogenesis. Methods: Non-atrophic gastritis (NAG) and chronic atrophic gastritis (CAG) patient pathology slides were collected, and related protein expression was detected by immunohistochemical staining. The CAG rat model was established using MNNG combined with an irregular diet. Results: CAG patients and rats exhibited iron deposition in gastric tissue. CAG-induced ferroptosis in the stomach was characterized by decreased GPX4 and FTH levels and increased 4-HNE levels. Hepcidin, which is mainly located in parietal cells, was elevated in CAG gastric tissue. The high gastric level of hepcidin inhibited iron absorption in the duodenum by decreasing the protein expression of DMT1 and FPN1. In addition, the IL-6/STAT3 signaling pathway induced hepcidin production in gastric tissue. Conclusion: Our results showed that the high level of gastric hepcidin induced ferroptosis in the stomach but also inhibited iron absorption in the intestines. Inhibiting hepcidin might be a new strategy for the prevention of CAG in the future. Full article
(This article belongs to the Special Issue Advances in Iron Deficiency and Iron-Related Disorders)
Show Figures

Graphical abstract

Back to TopTop