Cadmium disrupted homeostasis of proximal renal tubular cells via targeting ATF4-CHOP complex into the nucleus

Cadmium, a ubiquitous toxic metal and environmental pollutant, is associated with several renal metabolic disorders and disrupts the homeostasis of kidneys in humans and animals. However, the precise molecular mechanism remains poorly elucidated. The present study investigated the role of the ATF4-C...

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Main Authors: Muhammad Asmat Ullah Saleem, Ying-Xin Zhao, Farhat Bano, Yi-Xi Tang, Mu-Zi Li, Kanwar Kumar Malhi, Xiao-Wei Li, Xue-Nan Li, Yi Zhao, Jin-Long Li
Format: Article
Language:English
Published: Elsevier 2025-05-01
Series:Poultry Science
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Online Access:http://www.sciencedirect.com/science/article/pii/S0032579125002986
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author Muhammad Asmat Ullah Saleem
Ying-Xin Zhao
Farhat Bano
Yi-Xi Tang
Mu-Zi Li
Kanwar Kumar Malhi
Xiao-Wei Li
Xue-Nan Li
Yi Zhao
Jin-Long Li
author_facet Muhammad Asmat Ullah Saleem
Ying-Xin Zhao
Farhat Bano
Yi-Xi Tang
Mu-Zi Li
Kanwar Kumar Malhi
Xiao-Wei Li
Xue-Nan Li
Yi Zhao
Jin-Long Li
author_sort Muhammad Asmat Ullah Saleem
collection DOAJ
description Cadmium, a ubiquitous toxic metal and environmental pollutant, is associated with several renal metabolic disorders and disrupts the homeostasis of kidneys in humans and animals. However, the precise molecular mechanism remains poorly elucidated. The present study investigated the role of the ATF4-CHOP nuclear transcriptional axis and its interactions with cellular pathways in cadmium-induced nephrotoxicity. We acquired 120 one-day-old chickens, randomly divided them into four groups (Con, Cd35, Cd70, Cd140), and were treated with graded cadmium doses for 90 days. The kidney tissues were collected for comprehensive histopathological, biochemical, and molecular analyses using western blotting, qRT-PCR, immunofluorescence, and tunel assay. Subsequently, we revealed that cadmium exposure induced ER stress, significantly upregulated CHOP expression, and activated pro-apoptotic ATF4-CHOP axis. Our findings revealed a complex interplay, where ER stress activated inflammation. Concurrently, mitochondrial disruption elevated ROS production and oxidative stress, which impaired renal homeostasis. Moreover, inhibition of autophagy and mitophagy led to the accumulation of damaged cell organelles, further exacerbating apoptotic signaling. Our results elucidate that an integrated network of cellular stress pathways mediates cadmium-induced renal toxicity, with the ATF4-CHOP axis acting as a crucial pro-apoptotic pathway. This study provides critical insights into the mechanisms of cadmium-induced nephrotoxicity and potential therapeutic interventions to mitigate heavy metal-induced renal homeostasis disruption and renal damage.
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spelling doaj-art-d721c1c82b674f85b97d7a91b48c6b5f2025-08-20T03:10:21ZengElsevierPoultry Science0032-57912025-05-01104510505910.1016/j.psj.2025.105059Cadmium disrupted homeostasis of proximal renal tubular cells via targeting ATF4-CHOP complex into the nucleusMuhammad Asmat Ullah Saleem0Ying-Xin Zhao1Farhat Bano2Yi-Xi Tang3Mu-Zi Li4Kanwar Kumar Malhi5Xiao-Wei Li6Xue-Nan Li7Yi Zhao8Jin-Long Li9College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR ChinaCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR ChinaCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR ChinaCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR ChinaCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR ChinaCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR ChinaCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR ChinaCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China; Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin, 150030, PR China; Heilongjiang Key Laboratory for Laboratory Animals and Comparative Medicine, Northeast Agricultural University, Harbin, 150030, PR ChinaCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China; Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin, 150030, PR China; Heilongjiang Key Laboratory for Laboratory Animals and Comparative Medicine, Northeast Agricultural University, Harbin, 150030, PR ChinaCollege of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China; Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin, 150030, PR China; Heilongjiang Key Laboratory for Laboratory Animals and Comparative Medicine, Northeast Agricultural University, Harbin, 150030, PR China; Corresponding author at: College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China.Cadmium, a ubiquitous toxic metal and environmental pollutant, is associated with several renal metabolic disorders and disrupts the homeostasis of kidneys in humans and animals. However, the precise molecular mechanism remains poorly elucidated. The present study investigated the role of the ATF4-CHOP nuclear transcriptional axis and its interactions with cellular pathways in cadmium-induced nephrotoxicity. We acquired 120 one-day-old chickens, randomly divided them into four groups (Con, Cd35, Cd70, Cd140), and were treated with graded cadmium doses for 90 days. The kidney tissues were collected for comprehensive histopathological, biochemical, and molecular analyses using western blotting, qRT-PCR, immunofluorescence, and tunel assay. Subsequently, we revealed that cadmium exposure induced ER stress, significantly upregulated CHOP expression, and activated pro-apoptotic ATF4-CHOP axis. Our findings revealed a complex interplay, where ER stress activated inflammation. Concurrently, mitochondrial disruption elevated ROS production and oxidative stress, which impaired renal homeostasis. Moreover, inhibition of autophagy and mitophagy led to the accumulation of damaged cell organelles, further exacerbating apoptotic signaling. Our results elucidate that an integrated network of cellular stress pathways mediates cadmium-induced renal toxicity, with the ATF4-CHOP axis acting as a crucial pro-apoptotic pathway. This study provides critical insights into the mechanisms of cadmium-induced nephrotoxicity and potential therapeutic interventions to mitigate heavy metal-induced renal homeostasis disruption and renal damage.http://www.sciencedirect.com/science/article/pii/S0032579125002986CadmiumKidneyHomeostasisNephrotoxicityATF4-CHOP axis
spellingShingle Muhammad Asmat Ullah Saleem
Ying-Xin Zhao
Farhat Bano
Yi-Xi Tang
Mu-Zi Li
Kanwar Kumar Malhi
Xiao-Wei Li
Xue-Nan Li
Yi Zhao
Jin-Long Li
Cadmium disrupted homeostasis of proximal renal tubular cells via targeting ATF4-CHOP complex into the nucleus
Poultry Science
Cadmium
Kidney
Homeostasis
Nephrotoxicity
ATF4-CHOP axis
title Cadmium disrupted homeostasis of proximal renal tubular cells via targeting ATF4-CHOP complex into the nucleus
title_full Cadmium disrupted homeostasis of proximal renal tubular cells via targeting ATF4-CHOP complex into the nucleus
title_fullStr Cadmium disrupted homeostasis of proximal renal tubular cells via targeting ATF4-CHOP complex into the nucleus
title_full_unstemmed Cadmium disrupted homeostasis of proximal renal tubular cells via targeting ATF4-CHOP complex into the nucleus
title_short Cadmium disrupted homeostasis of proximal renal tubular cells via targeting ATF4-CHOP complex into the nucleus
title_sort cadmium disrupted homeostasis of proximal renal tubular cells via targeting atf4 chop complex into the nucleus
topic Cadmium
Kidney
Homeostasis
Nephrotoxicity
ATF4-CHOP axis
url http://www.sciencedirect.com/science/article/pii/S0032579125002986
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