Single-cell omics in tracing cellular heterogeneity of drug-induced liver injury: Technological landscape and prospective application

Mao, Xia; Xu, Mingzhu; Yan, Xiangying; Chen, Lin; Lin, Na; Zhang, Yanqiong

doi:10.1016/j.hlife.2024.01.004

Cited by 4 publications

(1 citation statement)

References 130 publications

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“…Additionally, the integration of omics technologies enhances the understanding of developmental toxicity mechanisms and facilitates biomarker discovery ( Mao et al, 2024 ). Integration of mass spectrometry with omics technologies and organoid models enhances assay precision, refining compound potency ranking in reprotoxicity tests.…”

Section: Advancements and Challenges In Assessing Developmental Toxicitymentioning

confidence: 99%

The reprotoxic adverse side effects of neurogenic and neuroprotective drugs: current use of human organoid modeling as a potential alternative to preclinical models

Abady,

Jeong,

Kwon

et al. 2024

Front. Pharmacol.

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The management of neurological disorders heavily relies on neurotherapeutic drugs, but notable concerns exist regarding their possible negative effects on reproductive health. Traditional preclinical models often fail to accurately predict reprotoxicity, highlighting the need for more physiologically relevant systems. Organoid models represent a promising approach for concurrently studying neurotoxicity and reprotoxicity, providing insights into the complex interplay between neurotherapeutic drugs and reproductive systems. Herein, we have examined the molecular mechanisms underlying neurotherapeutic drug-induced reprotoxicity and discussed experimental findings from case studies. Additionally, we explore the utility of organoid models in elucidating the reproductive complications of neurodrug exposure. Have discussed the principles of organoid models, highlighting their ability to recapitulate neurodevelopmental processes and simulate drug-induced toxicity in a controlled environment. Challenges and future perspectives in the field have been addressed with a focus on advancing organoid technologies to improve reprotoxicity assessment and enhance drug safety screening. This review underscores the importance of organoid models in unraveling the complex relationship between neurotherapeutic drugs and reproductive health.

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Section: Advancements and Challenges In Assessing Developmental Toxicitymentioning

confidence: 99%

The reprotoxic adverse side effects of neurogenic and neuroprotective drugs: current use of human organoid modeling as a potential alternative to preclinical models

Abady,

Jeong,

Kwon

et al. 2024

Front. Pharmacol.

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HiTIP-seq profiles epigenomic reprogramming of patient-derived diffuse midline glioma stem cells to epigenetic therapy

Chen,

Gao,

Shang

et al. 2024

hLife

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Polyploidy-mediated resilience in hepatic aging: molecular mechanisms and functional implication

Addissouky

2024

Egypt Liver Journal

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Background Polyploidization, a process where cells acquire additional chromosome sets, is a unique characteristic of hepatocytes. This process has been increasingly recognized as an adaptive mechanism for maintaining liver function during aging, a period characterized by cellular senescence, DNA damage, and metabolic dysregulation. Purpose This review explores the molecular mechanisms underlying hepatocyte polyploidization and its potential role in promoting resilience against the aging-related decline in liver function. We assess how polyploid hepatocytes contribute to genomic stability, stress resistance, and metabolic adaptation, highlighting their relevance to liver aging. Main body Hepatocyte polyploidization occurs through mechanisms such as cytokinesis failure and endoreplication, leading to binuclear or mononuclear polyploid cells. Polyploid hepatocytes exhibit enhanced DNA repair capacity, which helps mitigate the accumulation of age-related genomic damage. The increased gene dosage in polyploid cells facilitates better stress responses, particularly against oxidative stress and genotoxic insults. Metabolic adaptations, including enhanced xenobiotic metabolism and lipid regulation, further support the liver’s ability to maintain homeostasis during aging. Additionally, polyploid cells demonstrate altered epigenetic landscapes and proteostasis mechanisms, contributing to improved cellular function and reduced susceptibility to senescence. These adaptations collectively enhance liver resilience against age-related metabolic and structural challenges. Conclusion Hepatocyte polyploidization represents a critical protective mechanism in liver aging, promoting cellular adaptations that safeguard against genomic instability, metabolic dysfunction, and oxidative stress. Understanding the molecular pathways driving polyploidization could pave the way for novel therapeutic strategies to combat age-related liver disorders and enhance health span. Graphical Abstract

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Single-cell omics in tracing cellular heterogeneity of drug-induced liver injury: Technological landscape and prospective application

Cited by 4 publications

References 130 publications

The reprotoxic adverse side effects of neurogenic and neuroprotective drugs: current use of human organoid modeling as a potential alternative to preclinical models

The reprotoxic adverse side effects of neurogenic and neuroprotective drugs: current use of human organoid modeling as a potential alternative to preclinical models

HiTIP-seq profiles epigenomic reprogramming of patient-derived diffuse midline glioma stem cells to epigenetic therapy

Polyploidy-mediated resilience in hepatic aging: molecular mechanisms and functional implication

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