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Exploiting Mitochondria by Triggering a Faulty Unfolded Protein Response Leads to Effective Cardioprotection.
Int J Med Sci
January 2025
Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
This study investigates the role of Fundc1 in cardiac protection under high-altitude hypoxic conditions and elucidates its underlying molecular mechanisms. Using cardiomyocyte-specific knockout ( ) mice, we demonstrated that deficiency exacerbates cardiac dysfunction under simulated high-altitude hypoxia, manifesting as impaired systolic and diastolic function. Mechanistically, we identified that Fundc1 regulates cardiac function through the mitochondrial unfolded protein response (mito-UPR) pathway.
View Article and Find Full Text PDFFUNDC1 predicts Poor Prognosis and promotes Progression and Chemoresistance in Endometrial Carcinoma.
J Cancer
October 2024
Department of Gynecologic Oncology, Cancer Hospital of Shantou University Medical College, Shantou, China.
Absence of effective prognostic biomarkers and therapeutic targets for reversing chemoresistance of endometrial carcinoma (EC) remains a huge challenge for clinicians. Mitophagy plays a crucial role in carcinogenesis and chemoresistance. FUN14 domain-containing protein 1 (FUNDC1) is a novel mitophagy receptor protein involved in tumorigenesis under hypoxic conditions.
View Article and Find Full Text PDFEndothelial FUNDC1 Deficiency Drives Pulmonary Hypertension.
Circ Res
December 2024
State Key Laboratory of Medicinal Chemistry Biology, Haihe Laboratory of Cell Ecosystem, College of Life Sciences, Nankai University, China. (Y.P., D.R., Y.Y., J.S., Q.A., W.H., X. Luo, C.B., L. Zhu, Q.W., S.L., Y. Zhang, J.L., L.L., H.Z., Y.L., G.C., Q.C., X. Liao).
Background: Pulmonary hypertension (PH) is associated with endothelial dysfunction. However, the cause of endothelial dysfunction and its impact on PH remain incompletely understood. We aimed to investigate whether the hypoxia-inducible FUNDC1 (FUN14 domain-containing 1)-dependent mitophagy pathway underlies PH pathogenesis and progression.
View Article and Find Full Text PDFAdipoR1 promotes pathogenic Th17 differentiation by regulating mitochondrial function through FUNDC1.
J Biomed Res
November 2024
Department of Rheumatology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Adiponectin receptor 1 ( ) deficiency has been shown to inhibit Th17 cell differentiation and reduce joint inflammation and bone erosion in antigen-induced arthritis (AIA) mice. Additional emerging evidence indicates that Th17 cells may differentiate into pathogenic (pTh17) and non-pathogenic (npTh17) cells, with the pTh17 cells playing a crucial role in numerous autoimmune and inflammatory conditions. In the current study, we found that deficiency inhibited pTh17 differentiation and that the deletion of in pTh17 cells reduced the mitochondrial function.
View Article and Find Full Text PDFExploring the Mechanism of Ferroptosis Induction by Sappanone A in Cancer: Insights into the Mitochondrial Dysfunction Mediated by NRF2/xCT/GPX4 Axis.
Int J Biol Sci
October 2024
Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China.
Non-small cell lung cancer (NSCLC), a major subtype of lung cancer, encompasses squamous cell carcinoma, adenocarcinoma, and large cell carcinoma. Compared to small cell lung cancer, NSCLC cells grow and divide more slowly, and their metastasis occurs at a later stage. Currently, chemotherapy is the primary treatment for this disease.
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