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Skeletal muscle-derived musclin attenuates glycolysis, oxidative stress, and pulmonary hypertension through the NPR3/AKT/mTORC1 pathway.
Acta Biochim Biophys Sin (Shanghai)
December 2024
Department of Cardiovascular Medicine, the General Hospital of Western Theater Command, Chengdu 610083, China.
Exercise ameliorates pulmonary hypertension (PH) progression. However, the underlying mechanisms are largely unclear. Musclin is an exercise-responsive myokine that exerts protective effects on cardiovascular diseases.
View Article and Find Full Text PDFSerum proteome profiling reveals HGFA as a candidate biomarker for pulmonary arterial hypertension.
Respir Res
November 2024
National Center for Respiratory Medicine; State Key Laboratory of Respiratory Health and Multimorbidity; National Clinical Research Center for Respiratory Diseases; Institute of Respiratory Medicine, Chinese Academy of Medical Sciences; Department of Pulmonary and Critical Care Medicine, Center of Respiratory Medicine, China-Japan Friendship Hospital, Beijing, China.
Background: Identification and validation of potential biomarkers could facilitate the identification of pulmonary arterial hypertension (PAH) and thus aid to study their roles in the disease process.
Methods: We used the isobaric tag for relative and absolute quantitation approaches to compare the protein profiles between the serum of PAH patients and the controls. Bioinformatics analyses and enzyme-linked immunosorbent assay (ELISA) identification of PAH patients and the controls were performed to identify the potential biomarkers.
Article Synopsis
- The study aimed to explore if blocking the CCR2 receptor could prevent pulmonary arterial hypertension (PAH) in rat models and improve inflammatory and vascular issues.
- Researchers used genetically modified Ccr2(-/-) rats and found that these rats showed lower blood pressure in the heart, reduced inflammation, and less vascular damage after being exposed to certain treatments that typically induce PAH.
- Additionally, combining the CCR2 blockade with the PDE5 inhibitor tadalafil further improved symptoms of pulmonary hypertension, suggesting a potential therapeutic approach for PAH.
[Mechanism of vitamin D deficiency involvement in the development of pulmonary arterial hypertension related to monocrotaline-induced connective tissue disease in rats].
Zhonghua Yi Xue Za Zhi
November 2024
Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing210008, China.
To investigating the impact of vitamin D (VitD) deficiency on the jagged 1 protein (Jagged1)/Notch3 signaling pathway in the pulmonary arteries of rats with monocrotaline (MCT)-induced connective tissue disease (CTD)-related pulmonary arterial hypertension (PAH) and to explore the pathological and molecular mechanisms of VitD involvement in the development of CTD-PAH. Twenty-four 7-week-old male Wistar rats were divided into a normal diet group and a VitD-free diet group using random number table, with 12 rats in each group. After 5 weeks of feeding, the rats were further randomly divided into saline and MCT groups, forming group A (normal diet+saline), group B (normal diet+MCT), group C (VitD-free+saline), and group D (VitD-free+MCT), with 6 rats in each group, and the rats were continued to be fed for another 4 weeks.
View Article and Find Full Text PDFPI3K p85α/HIF-1α accelerates the development of pulmonary arterial hypertension by regulating fatty acid uptake and mitophagy.
Mol Med
November 2024
Cardiovascular Department, The Third Xiangya Hospital of Central South University, Changsha, 410013, China.
Background: Pulmonary arterial hypertension (PAH) is characterized by lipid accumulation and mitochondrial dysfunction. This study was designed to investigate the effects of hypoxia-inducible factor-1α (HIF-1α) on fatty acid uptake and mitophagy in PAH.
Methods: Peripheral blood samples were obtained from PAH patients.
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