Maduramicin ammonium impairs autophagic flux through activating AMPK‐mediated eIF2αATF4 endoplasmic reticulum stress pathway in skeletal muscle DOI Open Access
Xin Chen, Xin Xie, Chang Liu

et al.

Journal of the Science of Food and Agriculture, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 11, 2024

Maduramicin ammonium (MA), a widely used coccidiostat, has been reported to cause skeletal muscle degeneration in animals and even humans. In this study, we explore the underlying mechanism of its toxicity muscle.

Language: Английский

High glucose induces renal tubular epithelial cell senescence by inhibiting autophagic flux DOI
Ying Zhang, Yu Zhao, Yuqiu Liu

et al.

Human Cell, Journal Year: 2025, Volume and Issue: 38(2)

Published: Jan. 10, 2025

Language: Английский

Citations

2

Mechanisms of female reproductive toxicity in pigs induced by exposure to environmental pollutants DOI Open Access
Junho Park, Hojun Lee,

Junhun Kweon

et al.

Molecules and Cells, Journal Year: 2024, Volume and Issue: 47(5), P. 100065 - 100065

Published: April 26, 2024

Environmental pollutants, including endocrine disruptors, heavy metals, nanomaterials, and pesticides, have been detected in various ecosystems are of growing global concern. The potential for toxicity to non-target organisms has consistently raised is being studied using animal models. In this review, we focus on pesticides frequently the environment investigate their exposure livestock. Owing reproductive similarities between humans pigs, vitro porcine models such as oocytes, trophectoderm cells, luminal epithelial used verify toxicity. These cell lines study toxic mechanisms induced by environmental toxicants, organophosphate insecticides, pyrethroid dinitroaniline herbicides, diphenyl ether which persist threaten livestock health. Collectively, these results indicate that can induce female pigs suggest possibility adverse effects other species. also possible humans, requires further investigation.

Language: Английский

Citations

9

Brief guide to senescence assays using cultured mammalian cells DOI Open Access
Eun Seok Kang, Chanhee Kang, Young‐Sam Lee

et al.

Molecules and Cells, Journal Year: 2024, Volume and Issue: 47(9), P. 100102 - 100102

Published: July 23, 2024

Cellular senescence is a crucial biological process associated with organismal aging and many chronic diseases. Here, we present brief guide to mammalian assays, including the measurement of cell cycle arrest, change in cellular morphology, senescence-associated β-galactosidase (SA-β-gal) staining, expression secretory phenotype (SASP). This work will be useful for biologists minimum expertise assays.

Language: Английский

Citations

4

Propanil impairs organ development in zebrafish by inducing apoptosis and inhibiting mitochondrial respiration DOI
Taeyeon Hong, Jun Ho Park,

Nayoung Min

et al.

Journal of Hazardous Materials, Journal Year: 2024, Volume and Issue: 480, P. 136364 - 136364

Published: Oct. 31, 2024

Language: Английский

Citations

4

The Emerging Roles of Vacuolar-Type ATPase-Dependent Lysosomal Acidification in Cardiovascular Disease DOI Creative Commons
Yanyan Chen, Caixia Liu,

Hai‐Xin Liu

et al.

Biomolecules, Journal Year: 2025, Volume and Issue: 15(4), P. 525 - 525

Published: April 3, 2025

The vacuolar-type ATPase (V-ATPase) is a multi-subunit enzyme complex that maintains lysosomal acidification, critical process for cellular homeostasis. By controlling the pH within lysosomes, V-ATPase contributes to overall homeostasis, helping maintain balance between degradation and synthesis of components. Dysfunction impairs leading accumulation undigested materials contributing various diseases, including cardiovascular diseases (CVDs) like atherosclerosis myocardial disease. Furthermore, V-ATPase's role in function suggests potential therapeutic strategies targeting this mitigate disease progression. Understanding mechanisms by which influences pathology essential developing novel treatments aimed at improving outcomes patients with heart vascular diseases.

Language: Английский

Citations

0

Developmental and Organ Toxicity of Fenpropimorph in Zebrafish: Involvement of Apoptosis and Inflammation DOI

Junhun Kweon,

Hojun Lee, Jun Ho Park

et al.

Chemico-Biological Interactions, Journal Year: 2025, Volume and Issue: unknown, P. 111512 - 111512

Published: April 1, 2025

Language: Английский

Citations

0

Impacts of a high-glucose diet or starvation on microRNA-transcription factor networks in Caenorhabditis elegans through Boolean mathematical modeling DOI Creative Commons

Roberto Carlos Martinez-Padilla,

Luis Mendoza, Juan Miranda‐Ríos

et al.

Biosystems, Journal Year: 2025, Volume and Issue: unknown, P. 105503 - 105503

Published: May 1, 2025

Language: Английский

Citations

0

Brief guide to Caenorhabditis elegans survival assays DOI Open Access
H.C Kwon, Seung‐Jae Lee

Molecules and Cells, Journal Year: 2025, Volume and Issue: unknown, P. 100232 - 100232

Published: May 1, 2025

Language: Английский

Citations

0

Brief guide to assays for measuring health parameters using Caenorhabditis elegans DOI Open Access

Syh-Yuan Hwang,

Jongsun Lee,

Seung‐Jae Lee

et al.

Molecules and Cells, Journal Year: 2025, Volume and Issue: unknown, P. 100233 - 100233

Published: May 1, 2025

Language: Английский

Citations

0

Autophagy regulation and redox perturbation by transcrocetin suppress the growth of endometriosis DOI Open Access
Jiyeon Ham, Jisoo Song, Gwonhwa Song

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 173, P. 116284 - 116284

Published: Feb. 23, 2024

Until non-hormonal therapeutic targets for endometriosis are suggested, we focused on mitochondrial function and autophagy regulation in the disease. Transcrocetin is a carotenoid retinoic acid with high antioxidant potency antiproliferative effects several diseases. In this study, demonstrated mechanisms of transcrocetin using End1/E6E7 VK2/E6E7 cell lines. suppressed viability proliferation these lines did not affect normal uterine stromal cells. p21 Waf1/Cip1 as cycle regulator target p53, were increased by caused G1 arrest via inhibition cyclin-dependent kinase activity, which might further cause death. Furthermore, confirmed endoplasmic reticulum stress calcium ion dysregulation cytosol matrix, disrupting membrane potential. Mitochondrial bioenergetics transcrocetin, oxidative phosphorylation-related gene expression was downregulated. Moreover, cells regulated transcrocetin-induced stress. Finally, verified impairment autophagic flux following pre-treatment chloroquine. Therefore, may be potent alternative endometriosis.

Language: Английский

Citations

3