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Hepatic conditioning results in better lung endothelial cell preservation under hypoxic environment in vitro.
Int J Artif Organs
January 2025
Departments of Surgery and Bioengineering, McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA, USA.
Background: as we look to extend lung perfusion times (EVLP) to improve preservation, the metabolic activity of the lungs will require support from other organ functions. Active functional liver support, including detoxification, synthesis, and regulation, can improve lung preservation during EVLP. This study aimed to demonstrate the effects of hepatic conditioning of the EVLP perfusate on lung endothelium, via the receptor of advanced glycation end-products (RAGE)-nuclear-factor-κB (NF-κB) signaling in vitro.
View Article and Find Full Text PDFInhibition of NSUN6 protects against intermittent hypoxia-induced oxidative stress and inflammatory response in adipose tissue through suppressing macrophage ferroptosis and M1 polarization.
Life Sci
January 2025
Department of Orthopaedics, West China Hospital, Sichuan University, Chengdu, Sichuan, China. Electronic address:
Aims: Accumulating studies have demonstrated obstructive sleep apnea (OSA) is strongly associated with metabolic syndrome (MetS) and inflammatory response in adipose tissue. Chronic intermittent hypoxia (CIH) has been proved leading to M1 macrophage polarization that contributes to adipose tissue inflammation, but the molecular mechanism remains unclear. Epigenetic regulation of RNA has been found playing crucial roles in incremental diseases.
View Article and Find Full Text PDFMonocytes and interstitial macrophages contribute to hypoxic pulmonary hypertension.
J Clin Invest
January 2025
Department of Medicine, University of California San Francisco, San Francisco, United States of America.
Hypoxia is a major cause of pulmonary hypertension (PH) worldwide, and it is likely that interstitial pulmonary macrophages contribute to this vascular pathology. We observed in hypoxia-exposed mice an increase in resident interstitial macrophages, which expanded through proliferation and expressed the monocyte recruitment ligand CCL2. We also observed an increase in CCR2+ macrophages through recruitment, which express the protein thrombospondin-1 that functionally activates TGF-beta to cause vascular disease.
View Article and Find Full Text PDFMolecular and therapeutic insight into ER Stress signaling in NSCLC.
J Drug Target
January 2025
Department of Biotechnology and Bioengineering, Institute of Advanced Research, Gandhinagar, India.
Endoplasmic Reticulum (ER) stress is intricately involved in cancer development, progression and response to chemotherapy. ER stress related genes might play an important role in predicting the prognosis in lung adenocarcinoma patients and may be manipulated to improve the treatment outcome and overall survival rate. In this review, we analyzed the contribution of the three major ER stress pathways-IRE1, ATF6, and PERK-in lung cancer pathogenesis via modulation of tumor microenvironment (TME) and processes as metastasis, angiogenesis, apoptosis and N-glycosylation.
View Article and Find Full Text PDFMechanisms of (Fisch.) Bge. var. mongholicus (Bge.) Hsiao (huang qi) and (Oliv.) Diels (dang gui) in Ameliorating Hypoxia and Angiogenesis to Delay Pulmonary Nodule Malignant Transformation.
Integr Cancer Ther
January 2025
Affiliated Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Screening for pulmonary nodules (PN) using low-dose CT has proven effective in reducing lung cancer (LC) mortality. However, current treatments relying on follow-up and surgical excision fail to fully address clinical needs. Pathological angiogenesis plays a pivotal role in supplying oxygen necessary for the progression of PN to LC.
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