ABI3BP promotes renal aging through Klotho-mediated ferroptosis

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Abstract

The aging process of the kidneys is accompanied with several structural diseases. Abnormal fiber formation disrupts the balance of kidney structure and function, causing to end-stage renal disease and subsequent renal failure. Despite this, the precise mechanism underlying renal damage in aging remains elusive. In this study, ABI3BP gene knockout mice were used to investigate the role of ABI3BP in renal aging induced by irradiation. The results revealed a significant increase in ABI3BP expression in HK2 cells and kidney tissue of aging mice, with ABI3BP gene knockout demonstrating a mitigating effect on radiation-induced cell aging. Furthermore, the study observed a marked decrease in Klotho levels and an increase in ferroptosis in renal tissue and HK2 cells following irradiation. Notably, ABI3BP gene knockout not only elevated Klotho expression but also reduced ferroptosis levels. A significant negative correlation between ABI3BP and Klotho was established. Further experiments demonstrated that Klotho knockdown alleviated the aging inhibition caused by ABI3BP downregulation. This study identifies the upregulation of ABI3BP in aged renal tubular epithelial cells, indicating a role in promoting ferroptosis and inducing renal aging by inhibiting Klotho expression.

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Mutation of the mouse klotho gene leads to a syndrome resembling ageing.

M Kuro-O, Y Matsumura, H Aizawa … (1997)

A new gene, termed klotho, has been identified that is involved in the suppression of several ageing phenotypes. A defect in klotho gene expression in the mouse results in a syndrome that resembles human ageing, including a short lifespan, infertility, arteriosclerosis, skin atrophy, osteoporosis and emphysema. The gene encodes a membrane protein that shares sequence similarity with the beta-glucosidase enzymes. The klotho gene product may function as part of a signalling pathway that regulates ageing in vivo and morbidity in age-related diseases.

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Iron Metabolism in Ferroptosis

Xin Chen, Chunhua Yu, Rui Kang … (2020)

Ferroptosis is a form of regulated cell death that is characterized by iron-dependent oxidative damage and subsequent plasma membrane ruptures and the release of damage-associated molecular patterns. Due to the role of iron in mediating the production of reactive oxygen species and enzyme activity in lipid peroxidation, ferroptosis is strictly controlled by regulators involved in many aspects of iron metabolism, such as iron uptake, storage, utilization, and efflux. Translational and transcriptional regulation of iron homeostasis provide an integrated network to determine the sensitivity of ferroptosis. Impaired ferroptosis is implicated in various iron-related pathological conditions or diseases, such as cancer, neurodegenerative diseases, and ischemia-reperfusion injury. Understanding the molecular mechanisms underlying the regulation of iron metabolism during ferroptosis may provide effective strategies for the treatment of ferroptosis-associated diseases. Indeed, iron chelators effectively prevent the occurrence of ferroptosis, which may provide new approaches for the treatment of iron-related disorders. In this review, we summarize recent advances in the theoretical modeling of iron-dependent ferroptosis, and highlight the therapeutic implications of iron chelators in diseases.

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Renal Aging: Causes and Consequences.

Eoin O’Sullivan, Jeremy Hughes, David A Ferenbach (2017)

Individuals age >65 years old are the fastest expanding population demographic throughout the developed world. Consequently, more aged patients than before are receiving diagnoses of impaired renal function and nephrosclerosis-age-associated histologic changes in the kidneys. Recent studies have shown that the aged kidney undergoes a range of structural changes and has altered transcriptomic, hemodynamic, and physiologic behavior at rest and in response to renal insults. These changes impair the ability of the kidney to withstand and recover from injury, contributing to the high susceptibility of the aged population to AKI and their increased propensity to develop subsequent progressive CKD. In this review, we examine these features of the aged kidney and explore the various validated and putative pathways contributing to the changes observed with aging in both experimental animal models and humans. We also discuss the potential for additional study to increase understanding of the aged kidney and lead to novel therapeutic strategies.

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Author and article information

Contributors

Yan Ding:

ORCID: http://orcid.org/0000-0002-4269-9476

20090990@hbmu.edu.cn

Journal

Journal ID (nlm-ta): J Transl Med

Journal ID (iso-abbrev): J Transl Med

Title: Journal of Translational Medicine

Publisher: BioMed Central (London )

ISSN (Electronic): 1479-5876

Publication date (Electronic): 29 May 2024

Publication date PMC-release: 29 May 2024

Publication date Collection: 2024

Volume: 22

Electronic Location Identifier: 514

Affiliations

[1 ]GRID grid.443573.2, ISNI 0000 0004 1799 2448, Hubei Key Laboratory of Embryonic Stem Cell Research, Hubei Provincial Clinical Research Center for Umbilical Cord Blood Hematopoietic Stem Cells, Taihe Hospital, , Hubei University of Medicine, ; Shiyan, 442000 Hubei China

[2 ]Center for Clinical Laboratories, The Affiliated Hospital of Guizhou Medical University, ( https://ror.org/02kstas42) Guiyang, China

[3 ]GRID grid.443573.2, ISNI 0000 0004 1799 2448, Urology Department, Taihe Hospital, , Hubei University of Medicine, ; Shiyan, 442000 Hubei China

Author information

Yan Ding http://orcid.org/0000-0002-4269-9476

Article

Publisher ID: 5300

DOI: 10.1186/s12967-024-05300-w

PMC ID: 11134664

PubMed ID: 38812032

SO-VID: d205e343-d2ab-46f8-8173-eadb57d87d24

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Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 5 February 2024

Date accepted : 13 May 2024

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;

Award ID: 82270530

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ScienceOpen disciplines: Medicine

Keywords: abi3bp,renal aging,klotho,ferroptosis

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ScienceOpen disciplines: Medicine

Keywords: abi3bp, renal aging, klotho, ferroptosis

ABI3BP promotes renal aging through Klotho-mediated ferroptosis

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Aging Pathobiology and Therapeutics

Most cited references 32

Mutation of the mouse klotho gene leads to a syndrome resembling ageing.

Iron Metabolism in Ferroptosis

Renal Aging: Causes and Consequences.

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