DNA damage in proximal tubules triggers systemic metabolic dysfunction through epigenetically altered macrophages

Abstract DNA damage repair is a critical physiological process closely linked to aging. The accumulation of DNA damage in renal proximal tubular epithelial cells (PTEC) is related to a decline in kidney function. Here, we report that DNA double-strand breaks in PTECs lead to systemic metabolic dysfu...

Full description

Saved in:
Bibliographic Details
Main Authors: Erina Sugita Nishimura, Akihito Hishikawa, Ran Nakamichi, Riki Akashio, Shunsuke Chikuma, Akinori Hashiguchi, Norifumi Yoshimoto, Eriko Yoshida Hama, Tomomi Maruki, Wataru Itoh, Shintaro Yamaguchi, Jun Yoshino, Hiroshi Itoh, Kaori Hayashi
Format: Article
Language:English
Published: Nature Portfolio 2025-04-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-025-59297-x
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850284756243054592
author Erina Sugita Nishimura
Akihito Hishikawa
Ran Nakamichi
Riki Akashio
Shunsuke Chikuma
Akinori Hashiguchi
Norifumi Yoshimoto
Eriko Yoshida Hama
Tomomi Maruki
Wataru Itoh
Shintaro Yamaguchi
Jun Yoshino
Hiroshi Itoh
Kaori Hayashi
author_facet Erina Sugita Nishimura
Akihito Hishikawa
Ran Nakamichi
Riki Akashio
Shunsuke Chikuma
Akinori Hashiguchi
Norifumi Yoshimoto
Eriko Yoshida Hama
Tomomi Maruki
Wataru Itoh
Shintaro Yamaguchi
Jun Yoshino
Hiroshi Itoh
Kaori Hayashi
author_sort Erina Sugita Nishimura
collection DOAJ
description Abstract DNA damage repair is a critical physiological process closely linked to aging. The accumulation of DNA damage in renal proximal tubular epithelial cells (PTEC) is related to a decline in kidney function. Here, we report that DNA double-strand breaks in PTECs lead to systemic metabolic dysfunction, including weight loss, reduced fat mass, impaired glucose tolerance with mitochondrial dysfunction, and increased inflammation in adipose tissues and the liver. Single-cell RNA sequencing analysis reveals expansion of CD11c+ Ccr2+ macrophages in the kidney cortex, liver, and adipose tissues and Ly6Chi monocytes in peripheral blood. DNA damage in PTECs is associated with hypomethylation of macrophage activation genes, including Gasdermin D, in peripheral blood cells, which is linked to reduced DNA methylation at KLF9-binding motifs. Macrophage depletion ameliorates metabolic abnormalities. These findings highlight the impact of kidney DNA damage on systemic metabolic homeostasis, revealing a kidney-blood-metabolism axis mediated by epigenetic changes in macrophages.
format Article
id doaj-art-42fdef048d16492f93dedfb594d5b671
institution OA Journals
issn 2041-1723
language English
publishDate 2025-04-01
publisher Nature Portfolio
record_format Article
series Nature Communications
spelling doaj-art-42fdef048d16492f93dedfb594d5b6712025-08-20T01:47:29ZengNature PortfolioNature Communications2041-17232025-04-0116112010.1038/s41467-025-59297-xDNA damage in proximal tubules triggers systemic metabolic dysfunction through epigenetically altered macrophagesErina Sugita Nishimura0Akihito Hishikawa1Ran Nakamichi2Riki Akashio3Shunsuke Chikuma4Akinori Hashiguchi5Norifumi Yoshimoto6Eriko Yoshida Hama7Tomomi Maruki8Wataru Itoh9Shintaro Yamaguchi10Jun Yoshino11Hiroshi Itoh12Kaori Hayashi13Division of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of MedicineDivision of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of MedicineDivision of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of MedicineDivision of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of MedicineDepartment of Immunology, Keio University School of MedicineDepartment of Pathology, Keio University School of MedicineDivision of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of MedicineDivision of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of MedicineDivision of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of MedicineDivision of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of MedicineSchool of Medicine Medical Education Center, Keio UniversityDivision of Nephrology, Department of Internal Medicine, Faculty of Medicine, Shimane UniversityCenter for Preventive Medicine, Keio University HospitalDivision of Nephrology, Endocrinology and Metabolism, Department of Internal Medicine, Keio University School of MedicineAbstract DNA damage repair is a critical physiological process closely linked to aging. The accumulation of DNA damage in renal proximal tubular epithelial cells (PTEC) is related to a decline in kidney function. Here, we report that DNA double-strand breaks in PTECs lead to systemic metabolic dysfunction, including weight loss, reduced fat mass, impaired glucose tolerance with mitochondrial dysfunction, and increased inflammation in adipose tissues and the liver. Single-cell RNA sequencing analysis reveals expansion of CD11c+ Ccr2+ macrophages in the kidney cortex, liver, and adipose tissues and Ly6Chi monocytes in peripheral blood. DNA damage in PTECs is associated with hypomethylation of macrophage activation genes, including Gasdermin D, in peripheral blood cells, which is linked to reduced DNA methylation at KLF9-binding motifs. Macrophage depletion ameliorates metabolic abnormalities. These findings highlight the impact of kidney DNA damage on systemic metabolic homeostasis, revealing a kidney-blood-metabolism axis mediated by epigenetic changes in macrophages.https://doi.org/10.1038/s41467-025-59297-x
spellingShingle Erina Sugita Nishimura
Akihito Hishikawa
Ran Nakamichi
Riki Akashio
Shunsuke Chikuma
Akinori Hashiguchi
Norifumi Yoshimoto
Eriko Yoshida Hama
Tomomi Maruki
Wataru Itoh
Shintaro Yamaguchi
Jun Yoshino
Hiroshi Itoh
Kaori Hayashi
DNA damage in proximal tubules triggers systemic metabolic dysfunction through epigenetically altered macrophages
Nature Communications
title DNA damage in proximal tubules triggers systemic metabolic dysfunction through epigenetically altered macrophages
title_full DNA damage in proximal tubules triggers systemic metabolic dysfunction through epigenetically altered macrophages
title_fullStr DNA damage in proximal tubules triggers systemic metabolic dysfunction through epigenetically altered macrophages
title_full_unstemmed DNA damage in proximal tubules triggers systemic metabolic dysfunction through epigenetically altered macrophages
title_short DNA damage in proximal tubules triggers systemic metabolic dysfunction through epigenetically altered macrophages
title_sort dna damage in proximal tubules triggers systemic metabolic dysfunction through epigenetically altered macrophages
url https://doi.org/10.1038/s41467-025-59297-x
work_keys_str_mv AT erinasugitanishimura dnadamageinproximaltubulestriggerssystemicmetabolicdysfunctionthroughepigeneticallyalteredmacrophages
AT akihitohishikawa dnadamageinproximaltubulestriggerssystemicmetabolicdysfunctionthroughepigeneticallyalteredmacrophages
AT rannakamichi dnadamageinproximaltubulestriggerssystemicmetabolicdysfunctionthroughepigeneticallyalteredmacrophages
AT rikiakashio dnadamageinproximaltubulestriggerssystemicmetabolicdysfunctionthroughepigeneticallyalteredmacrophages
AT shunsukechikuma dnadamageinproximaltubulestriggerssystemicmetabolicdysfunctionthroughepigeneticallyalteredmacrophages
AT akinorihashiguchi dnadamageinproximaltubulestriggerssystemicmetabolicdysfunctionthroughepigeneticallyalteredmacrophages
AT norifumiyoshimoto dnadamageinproximaltubulestriggerssystemicmetabolicdysfunctionthroughepigeneticallyalteredmacrophages
AT erikoyoshidahama dnadamageinproximaltubulestriggerssystemicmetabolicdysfunctionthroughepigeneticallyalteredmacrophages
AT tomomimaruki dnadamageinproximaltubulestriggerssystemicmetabolicdysfunctionthroughepigeneticallyalteredmacrophages
AT wataruitoh dnadamageinproximaltubulestriggerssystemicmetabolicdysfunctionthroughepigeneticallyalteredmacrophages
AT shintaroyamaguchi dnadamageinproximaltubulestriggerssystemicmetabolicdysfunctionthroughepigeneticallyalteredmacrophages
AT junyoshino dnadamageinproximaltubulestriggerssystemicmetabolicdysfunctionthroughepigeneticallyalteredmacrophages
AT hiroshiitoh dnadamageinproximaltubulestriggerssystemicmetabolicdysfunctionthroughepigeneticallyalteredmacrophages
AT kaorihayashi dnadamageinproximaltubulestriggerssystemicmetabolicdysfunctionthroughepigeneticallyalteredmacrophages