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Pathophysiology
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Physiology of Iron Metabolism
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Physiology of Iron Metabolism

A special issue of Pathophysiology (ISSN 1873-149X).

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 7786

Special Issue Editor

Dr. Nupur Das

E-Mail Website
Guest Editor
Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, USA
Interests: iron deficiency; hemochromatosis; hypoxia inducible factors; PCBPs; ferritinophagy; host-gut microbiota crosstalk; ferroptosis; iron regulatory proteins; hemoglobinopathies; cancer; infection; COVID-19
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Iron is the second most abundant metal and the fourth most abundant element of the earth’s crust. It is essential for numerous biochemical processes of almost every organism, such as oxygen sensing and transport, electron transfer, and catalysis. Therefore, adequate iron supply is critical for cellular as well as organismal homeostasis. Although iron deficiency leads to various biochemical disorders, iron excess is potentially toxic as it can generate reactive oxygen species (ROS) via Fenton reactions. Organisms of different orders have thus developed customized iron metabolism of their own which has to be tightly regulated. Regular and sufficient intake of iron through diet is critical for efficient hemoglobin synthesis in the mammals. In humans, iron imbalance constitutes a major global health burden, as both deficiency (mainly nutritional) and overload (genetically encoded) disorders are prevalent in distinct geographical and genetic backgrounds. In addition, dysregulated iron metabolism has been implicated in various disorders, such as inflammation, infection, and cancer highlighting its much broader role in pathophysiology. Over recent years, discovery of several new players in cellular and systemic iron regulation has revolutionized our understandings from both basic science and translational perspectives. For example, novel roles of host-gut microbiota crosstalk in mammalian iron homeostasis, and its connection with cell proliferation and metabolism have generated widespread interest. Many questions still remain unanswered with regard to the organellar dynamics of iron in cellular physiology, for which ongoing studies and relentless efforts are currently under way.

Dr. Nupur Das
Guest Editor

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Keywords

  • Iron deficiency
  • Hemochromatosis
  • Hypoxia inducible factors
  • PCBPs
  • Ferritinophagy
  • Host-gut microbiota crosstalk
  • Ferroptosis
  • Iron regulatory proteins
  • Hemoglobinopathies
  • Cancer
  • Infection
  • COVID-19

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Published Papers (2 papers)

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Research

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12 pages, 2501 KiB  
Article
Ferritin, Serum Iron and Hemoglobin as Acute Phase Reactants in Laparoscopic and Open Surgery of Cholecystectomy: An Observational Prospective Study
by Cristina Vila Zárate, Candelaria Martín González, Ruimán José González Álvarez, Iván Soto Darias, Beatriz Díaz Pérez, Pedro Abreu González, Vicente Medina Arana and Antonio Martínez Riera
Pathophysiology 2022, 29(4), 583-594; https://doi.org/10.3390/pathophysiology29040045 - 11 Oct 2022
Cited by 3 | Viewed by 3324
Abstract
Cytokines are expressed by various cells after several stimuli such as surgical tissue damage, producing a systemic inflammatory response (SIR). C-reactive protein (CRP) is used extensively in clinical practice after operative injury, but proinflammatory cytokines, iron status, albumin, neutrophil-to-lymphocyte (N/L) ratio and hemoglobin, [...] Read more.
Cytokines are expressed by various cells after several stimuli such as surgical tissue damage, producing a systemic inflammatory response (SIR). C-reactive protein (CRP) is used extensively in clinical practice after operative injury, but proinflammatory cytokines, iron status, albumin, neutrophil-to-lymphocyte (N/L) ratio and hemoglobin, as acute phase reactants, have been poorly documented. This study aims to show how they behave after surgery, comparing laparoscopic (LC) versus open cholecystectomy (OC). In total, 55 patients were included in a prospective non-randomized form to undergo a cholecystectomy: 8 patients OC (50% females) and 47 patients LC (68% females). Before (A1) and 24 h after surgery (A2), blood samples were taken for an ordinary analysis and IL6, IL8 and TNFα determination. There were no differences between LC and OC groups concerning age, CRP, IL6 and TNFα at day A1. In the LC group at day A2, CRP, IL6, IL8, TNF, ferritin, leukocytes and N/L ratio increased; hemoglobin, lymphocytes, prothrombin and albumin decreased (p < 0.05). In the OC group at day A2, only IL6 (p < 0,07), ferritin, leukocytes, N/L ratio and CRP (p < 0.05) increased; serum iron, hemoglobin, lymphocytes and albumin (p < 0.05) decreased. At day A2, OC vs. LC group, higher values were observed in IL6, ferritin and CRP (p ≤ 0.05), and lesser values were observed in serum iron and prothrombin (p < 0.05). In conclusion, classic markers of inflammation are altered after surgery, in a milder way in laparoscopic surgery. Ferritin can be used as an inflammatory marker, as has been described in COVID-19 infection. Full article
(This article belongs to the Special Issue Physiology of Iron Metabolism)
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Review

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20 pages, 2998 KiB  
Review
The Emerging Role of Heat Shock Factor 1 (HSF1) and Heat Shock Proteins (HSPs) in Ferroptosis
by Iman Aolymat, Ma’mon M. Hatmal and Amin N. Olaimat
Pathophysiology 2023, 30(1), 63-82; https://doi.org/10.3390/pathophysiology30010007 - 14 Mar 2023
Cited by 12 | Viewed by 3674
Abstract
Cells employ a well-preserved physiological stress response mechanism, termed the heat shock response, to activate a certain type of molecular chaperone called heat shock proteins (HSPs). HSPs are activated by transcriptional activators of heat shock genes known as heat shock factors (HSFs). These [...] Read more.
Cells employ a well-preserved physiological stress response mechanism, termed the heat shock response, to activate a certain type of molecular chaperone called heat shock proteins (HSPs). HSPs are activated by transcriptional activators of heat shock genes known as heat shock factors (HSFs). These molecular chaperones are categorized as the HSP70 superfamily, which includes HSPA (HSP70) and HSPH (HSP110) families; the DNAJ (HSP40) family; the HSPB family (small heat shock proteins (sHSPs)); chaperonins and chaperonin-like proteins; and other heat-inducible protein families. HSPs play a critical role in sustaining proteostasis and protecting cells against stressful stimuli. HSPs participate in folding newly synthesized proteins, holding folded proteins in their native conformation, preventing protein misfolding and accumulation, and degrading denatured proteins. Ferroptosis is a recently identified type of oxidative iron-dependent cell demise. It was coined recently in 2012 by Stockwell Lab members, who described a special kind of cell death induced by erastin or RSL3. Ferroptosis is characterized by alterations in oxidative status resulting from iron accumulation, increased oxidative stress, and lipid peroxidation, which are mediated by enzymatic and non-enzymatic pathways. The process of ferroptotic cell death is regulated at multiple, and it is involved in several pathophysiological conditions. Much research has emerged in recent years demonstrating the involvement of HSPs and their regulator heat shock factor 1 (HSF1) in ferroptosis regulation. Understanding the machinery controlling HSF1 and HSPs in ferroptosis can be employed in developing therapeutic interventions for ferroptosis occurrence in a number of pathological conditions. Therefore, this review comprehensively summarized the basic characteristics of ferroptosis and the regulatory functions of HSF1 and HSPs in ferroptosis. Full article
(This article belongs to the Special Issue Physiology of Iron Metabolism)
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