Iron: an underrated factor in aging

Mangan, D F

doi:10.18632/aging.203612

Cited by 23 publications

(18 citation statements)

References 73 publications

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“…Specifically, activation of mTOR leads to an increase in body iron levels, which in turn activates mTOR. Therefore, one of the mechanisms inhibiting mTOR in prolonging lifespan may be through inhibiting body iron levels [ 84 ]. In addition, ferroptosis is an iron-dependent, nonapoptotic programmed cell death.…”

Section: Iron Metabolism and Agingmentioning

confidence: 99%

Iron Metabolism in Aging and Age-Related Diseases

Tian

Yuan

et al. 2022

IJMS

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Iron is a trace metal element necessary to maintain life and is also involved in a variety of biological processes. Aging refers to the natural life process in which the physiological functions of the various systems, organs, and tissues decline, affected by genetic and environmental factors. Therefore, it is imperative to investigate the relationship between iron metabolism and aging-related diseases, including neurodegenerative diseases. During aging, the accumulation of nonheme iron destroys the stability of the intracellular environment. The destruction of iron homeostasis can induce cell damage by producing hydroxyl free radicals, leading to mitochondrial dysfunction, brain aging, and even organismal aging. In this review, we have briefly summarized the role of the metabolic process of iron in the body, then discussed recent developments of iron metabolism in aging and age-related neurodegenerative diseases, and finally, explored some iron chelators as treatment strategies for those disorders. Understanding the roles of iron metabolism in aging and neurodegenerative diseases will fill the knowledge gap in the field. This review could provide new insights into the research on iron metabolism and age-related neurodegenerative diseases.

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Section: Iron Metabolism and Agingmentioning

confidence: 99%

Iron Metabolism in Aging and Age-Related Diseases

Tian

Yuan

et al. 2022

IJMS

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“…Interestingly, as CatB possesses endopeptidase activity, the SARS-CoV-2 virus hijacks this protein to activate the S (spike) antigen, increasing infectivity ( Schornberg et al, 2006 ; Mitrović et al, 2016 ; Huang et al, 2020 ; Padmanabhan et al, 2020 ). Moreover, individuals with HIV-1 infection on long-term cART present with higher brain deposition of pTau, linking this virus and its treatment to the risk of developing tauopathies ( Anthony et al, 2006 ; Brown et al, 2014 ; Rao and Adlard, 2018 ; Mangan, 2021 ). These findings indicate that HIV-1 and CART induce lysosomal damage and predispose to FIN as elevated intracellular iron increases the odds of lipid peroxidation and ferroptotic cell death ( Jiang et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Bromodomains in Human-Immunodeficiency Virus-Associated Neurocognitive Disorders: A Model of Ferroptosis-Induced Neurodegeneration

et al. 2022

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Graphical AbstractBoth HIV-1 and cART alter the lysosomes, increasing intracellular iron and the risk of ferroptosis. Dysfunctional lysosomes release the ferroptosis drivers iron, Ca2+ and cathepsin B (catB), promoting neuronal and oligodendrocyte loss, reflected in the white and gray matter pathology. The host responds to lysosomal damage by activating an epigenetic axis comprised of bromodomain 4 (BRD4) and microRNA-29 family (miR-29) that promptly suppresses lysosomal function, lowering ferritinophagy. As there is an inverse relationship between miR-29 and BRD4, HIV-1 inhibition of miR-29, upregulates BRD4, blocking ferritinophagy. The BRD4/miR-29 system also inhibits iron regulatory protein-2 (IRP-2) and augments cystine/glutamate antiporter xCT (SLC7A11), lowering the odds of ferroptosis.

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“…Although age, mechanical load, and joint injury are the primary risk factors, pathophysiology and internal mechanisms associated with OA have not been fully explored (Shane Anderson and Loeser, 2010;Courties et al, 2015). During the aging process, iron accumulates in various tissues and organs due to the lack of the main mechanism of iron excretion in the human body (Mangan, 2021). Thus, it is speculated that the degenerative cartilage changes in middle-aged and elderly patients with OA may be related to iron overload in the joints.…”

Section: Aging-and Estrogen Deficiency-induced Osteoarthritismentioning

confidence: 99%

Interplay Between Iron Overload and Osteoarthritis: Clinical Significance and Cellular Mechanisms

Cai

Chu

2022

Front. Cell Dev. Biol.

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There are multiple diseases or conditions such as hereditary hemochromatosis, hemophilia, thalassemia, sickle cell disease, aging, and estrogen deficiency that can cause iron overload in the human body. These diseases or conditions are frequently associated with osteoarthritic phenotypes, such as progressive cartilage degradation, alterations in the microarchitecture and biomechanics of the subchondral bone, persistent joint inflammation, proliferative synovitis, and synovial pannus. Growing evidences suggest that the conditions of pathological iron overload are associated with these osteoarthritic phenotypes. Osteoarthritis (OA) is an important complication in patients suffering from iron overload-related diseases and conditions. This review aims to summarize the findings and observations made in the field of iron overload-related OA while conducting clinical and basic research works. OA is a whole-joint disease that affects the articular cartilage lining surfaces of bones, subchondral bones, and synovial tissues in the joint cavity. Chondrocytes, osteoclasts, osteoblasts, and synovial-derived cells are involved in the disease. In this review, we will elucidate the cellular and molecular mechanisms associated with iron overload and the negative influence that iron overload has on joint homeostasis. The promising value of interrupting the pathologic effects of iron overload is also well discussed for the development of improved therapeutics that can be used in the field of OA.

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Iron: an underrated factor in aging

Cited by 23 publications

References 73 publications

Iron Metabolism in Aging and Age-Related Diseases

Iron Metabolism in Aging and Age-Related Diseases

Bromodomains in Human-Immunodeficiency Virus-Associated Neurocognitive Disorders: A Model of Ferroptosis-Induced Neurodegeneration

Interplay Between Iron Overload and Osteoarthritis: Clinical Significance and Cellular Mechanisms

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