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epithelial cells

Sensitization of the UPR by Loss of PPP1R15A Promotes Fibrosis and Senescence in IPF

[Scientific Reports] Researchers demonstrated the major role of PPP1R15A in the regulation of lung mesenchymal cells, and regulation of PPP1R15A may represent a novel therapeutic strategy in idiopathic pulmonary fibrosis.

Management of Intrauterine Adhesions Using Human Amniotic Mesenchymal Stromal Cells to Promote Endometrial Regeneration and Repair through Notch Signaling

[Journal of Cellular and Molecular Medicine] Investigators examined the function of Notch signaling in intrauterine adhesions treatment with human amniotic mesenchymal stromal cell (hAMSC) transplantation, and found that it mediated the differentiation of hAMSCs into endometrial epithelial cells, thus promoting endometrial regeneration and repair.

Molecular Programs of Fibrotic Change in Aging Human Lung

[Nature Communications] Researchers profiled distal lung samples from healthy human donors across the lifespan and revealed the transcriptional and structural features of fibrosis and associated functional impairment in normal lung aging.

Role of Lysocardiolipin Acyltransferase in Cigarette Smoke-Induced Lung Epithelial Cell Mitochondrial ROS, Mitochondrial Dynamics, and Apoptosis

[Cell Biochemistry and Biophysics] Researchers investigated the role of lysocardiolipin acyltransferase expression and activity in mitochondrial oxidative stress, mitochondrial dynamics, and lung epithelial cell apoptosis.

Nrf2 Attenuates Ferroptosis-Mediated IIR-ALI by Modulating TERT and SLC7A11

[Cell Death & Disease] Researchers found that telomerase reverse transcriptase (TERT) was significantly reduced in lung tissue of Nrf2−/− mice in the model of intestinal ischemia/reperfusion-induced acute lung injury (IIR-ALI)

Endothelial Cells Are Not Productively Infected by SARS-CoV-2

[Clinical & Translational Immunology] Researchers showed that primary human endothelial cells expressed very low levels of the SARS-CoV-2 receptor ACE2 and the protease TMPRSS2, which blocked their capacity for productive viral infection, and limited their capacity to produce infectious virus.

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