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Promoting epithelial regeneration in chemically induced acute lung injury through Sox9-positive alveolar type 2 epithelial cells.
Stem Cell Res Ther
January 2025
Center of Emergency and Critical Medicine, Jinshan Hospital of Fudan University, Shanghai, People's Republic of China.
Background: Chemical-induced acute lung injury is characterized by impaired epithelial regenerative capacity, leading to acute pulmonary edema. Numerous studies have investigated the therapeutic potential of endogenous stem cells with particular emphasis on alveolar type 2 epithelial (AEC2) cells owing to their involvement in lung cell renewal. Sox9, a transcription factor known for its role in maintaining stem cell properties and guiding cell differentiation, marks a subset of AEC2 cells believed to contribute to epithelial repair.
View Article and Find Full Text PDFQuantifying liver-toxic responses from dose-dependent chemical exposures using a rat genome-scale metabolic model.
Toxicol Sci
January 2025
Department of Defense Biotechnology High Performance Computing Software Applications Institute, Telemedicine and Advanced Technology Research Center, U.S. Army Medical Research and Development Command, Fort Detrick, MD, 21702, USA.
Because the liver plays a vital role in the clearance of exogenous chemical compounds, it is susceptible to chemical-induced toxicity. Animal-based testing is routinely used to assess the hepatotoxic potential of chemicals. While large-scale high-throughput sequencing data can indicate the genes affected by chemical exposures, we need system-level approaches to interpret these changes.
View Article and Find Full Text PDFModelling the combined effects of ionising radiation and chemical pollutants on wildlife populations.
J Environ Radioact
January 2025
Belgian Nuclear Research Centre (SCK CEN), Boeretang 200, 2400 Mol, Belgium. Electronic address:
A population model is presented to study the combined effects of ionising radiation and chemical pollutants on wildlife. The model is based on first order, non-linear and logistic differential equations combining mortality, morbidity and reproduction phenomena with life history data and ecological interactions. Acclimation is considered as a possible mechanism to study theoretically this effect at low levels of radiation or chemical concentration.
View Article and Find Full Text PDFStructure-Based Design of "Head-to-Tail" Macrocyclic PROTACs.
JACS Au
December 2024
State Key Laboratory of Chemical Biology, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, No. 345 Lingling Road, Shanghai 200032, China.
Macrocyclization is a compelling strategy for conventional drug design for improving biological activity, target specificity, and metabolic stability, but it was rarely applied to the design of PROTACs possibly due to the mechanism and structural complexity. Herein, we report the rational design of the first series of "Head-to-Tail" macrocyclic PROTACs. The resulting molecule exhibited pronounced Brd4 protein degradation with low nM DC values while almost totally dismissing the "hook effect", which is a general character and common concern of a PROTAC, in multiple cancer cell lines.
View Article and Find Full Text PDFKCNJ15 inhibits chemical-induced lung carcinogenesis and progression through GNB1 mediated Hippo pathway.
Toxicology
December 2024
Department of Environmental Health, College of Preventive Medicine, Third Military Medical University (Army Medical University), Chongqing 400038, China; Institute of Toxicology, College of Preventive Medicine, Third Military Medical University (Army Medical University), Chongqing 400038, China. Electronic address:
Polycyclic aromatic hydrocarbons (PAHs) are important environmental carcinogens that can cause lung cancer. However, the underlying epigenetic mechanism during PAHs-induced lung carcinogenesis has remained largely unknown. Previously, we screened some novel epigenetic regulatory genes during 3-methylcholanthrene (3-MCA)-induced lung carcinogenesis, including the potassium inwardly rectifying channel subfamily J member 15 (KCNJ15) gene.
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