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Article ; Online: Beclin 1

Zeng, Xiaofang / Sun, Jing / Li, Famei / Peng, Liming / Zhang, Chenglong / Jiang, Xiaowei / Zha, Lihuang / Rathinasabapathy, Anandharajan / Ren, Jun / Yu, Zaixin / Wang, Lin / Liu, Xiangwei

Antioxidants & redox signaling

2024

Abstract: Aims: ...

Abstract	Aims:
Language	English
Publishing date	2024-03-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2023.0399
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Article: Ubiquitin chains: a new way of screening for regulatory differences in pulmonary hypertension.

Rathinasabapathy, Anandharajan / West, James D

Pulmonary circulation

2018 Volume 8, Issue 3, Page(s) 2045894018796782

Abstract: Protein ubiquitination serves many regulatory functions; in addition to degradation, ubiquitination has roles in intracellular trafficking, cell cycle, innate immunity, and more. Using mass spectrometry, it is possible to assess the ubiquitination state ... ...

Abstract	Protein ubiquitination serves many regulatory functions; in addition to degradation, ubiquitination has roles in intracellular trafficking, cell cycle, innate immunity, and more. Using mass spectrometry, it is possible to assess the ubiquitination state of every protein simultaneously. In this issue, Wade et al. have for the first time done just that in a hypoxic mouse model of pulmonary hypertension (PH). New techniques drive new discoveries; their work is important not just because they have found new ways to intervene in known PH-related pathways but have found regulation of proteins not previously associated with disease.
Language	English
Publishing date	2018-08-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2638089-4
ISSN	2045-8940 ; 2045-8932
ISSN (online)	2045-8940
ISSN	2045-8932
DOI	10.1177/2045894018796782
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Article ; Online: Pulmonary veno-occlusive disease in Sjogren's syndrome: a case report.

Zeng, Xiaofang / Liu, Qiong / Rathinasabapathy, Anandharajan / Zha, Lihuang / Liu, Dongliang / Tang, Yiyang / Sun, Jing / Luo, Hui / Yu, Zaixin

BMC pulmonary medicine

2023 Volume 23, Issue 1, Page(s) 26

Abstract: Background: Pulmonary arterial hypertension (PAH) associated with connective tissue disease (CTD) belongs to Group 1 pulmonary hypertension. Pulmonary veno-occlusive disease (PVOD), which is characterized by venous system aberrations, has been ... ...

Abstract	Background: Pulmonary arterial hypertension (PAH) associated with connective tissue disease (CTD) belongs to Group 1 pulmonary hypertension. Pulmonary veno-occlusive disease (PVOD), which is characterized by venous system aberrations, has been previously reported in CTD-PAH; however, it has rarely been observed in Sjogren's syndrome (SS). Case presentation: Our 28-year-old female patient was admitted to the hospital with recurrent shortness of breath even after minimal physical activity. Her chest high-resolution CT scan demonstrated pulmonary artery dilatation and bilateral ground-glass nodules. A subsequent right heart catheterization confirmed pulmonary hypertension because her mean pulmonary arterial pressure was 62 mmHg. Our inquisitive genomic assessment identified a novel EIF2AK4 mutation at c.1021 C > T (p. Gln341), the dominant causal gene of PVOD. Histological examination demonstrated stenosis and occlusions in the pulmonary veins. Because she presented with features such as dry eyes and Raynaud's phenomenon, we performed a biopsy on the labial salivary gland, which confirmed SS. Her treatment regimen included PAH-targeted therapies (tadalafil and macitentan) in combination with hydroxychloroquine. Although she was hospitalized several times due to acute exacerbation of PAH, her disease progression was under control, and she did not demonstrate any signs of pulmonary edema even after a three-year treatment period. Conclusion:* Here, we report the case of an SS-PAH patient with PVOD who carried a novel biallelic EIF2AK4 mutation, and PAH-targeted therapies were well tolerated by our patient.
MeSH term(s)	Humans ; Female ; Adult ; Hypertension, Pulmonary ; Pulmonary Veno-Occlusive Disease/complications ; Pulmonary Veno-Occlusive Disease/diagnosis ; Pulmonary Veno-Occlusive Disease/genetics ; Sjogren's Syndrome/complications ; Sjogren's Syndrome/genetics ; Lung ; Pulmonary Arterial Hypertension ; Familial Primary Pulmonary Hypertension ; Protein Serine-Threonine Kinases/genetics
Chemical Substances	EIF2AK4 protein, human (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2023-01-18
Publishing country	England
Document type	Case Reports ; Journal Article
ZDB-ID	2059871-3
ISSN	1471-2466 ; 1471-2466
ISSN (online)	1471-2466
ISSN	1471-2466
DOI	10.1186/s12890-023-02322-w
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Article ; Online: Prevalence of

Zeng, Xiaofang / Huang, Xiao / Rathinasabapathy, Anandharajan / Xu, Zhe / Li, Kai / Liu, Na / Chen, Huiling / Jiang, Yuandong / Zha, Lihuang / Yu, Zaixin

Annals of the American Thoracic Society

2021 Volume 18, Issue 12, Page(s) 2095–2098

MeSH term(s)	Animals ; China/epidemiology ; Echocardiography ; Humans ; Hypertension, Pulmonary/diagnostic imaging ; Hypertension, Pulmonary/epidemiology ; Prevalence ; Schistosoma japonicum
Language	English
Publishing date	2021-06-28
Publishing country	United States
Document type	Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2717461-X
ISSN	2325-6621 ; 1943-5665 ; 2325-6621
ISSN (online)	2325-6621 ; 1943-5665
ISSN	2325-6621
DOI	10.1513/AnnalsATS.202012-1573RL
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Article ; Online: Overexpression of Msx1 in Mouse Lung Leads to Loss of Pulmonary Vessels Following Vascular Hypoxic Injury.

West, James / Rathinasabapathy, Anandharajan / Chen, Xinping / Shay, Sheila / Gladson, Shanti / Talati, Megha

Cells

2021 Volume 10, Issue 9

Abstract: Pulmonary arterial hypertension (PAH) is a progressive lung disease caused by thickening of the pulmonary arterial wall and luminal obliteration of the small peripheral arteries leading to increase in vascular resistance which elevates pulmonary artery ... ...

Abstract	Pulmonary arterial hypertension (PAH) is a progressive lung disease caused by thickening of the pulmonary arterial wall and luminal obliteration of the small peripheral arteries leading to increase in vascular resistance which elevates pulmonary artery pressure that eventually causes right heart failure and death. We have previously shown that transcription factor Msx1 (mainly expressed during embryogenesis) is strongly upregulated in transformed lymphocytes obtained from PAH patients, especially IPAH. Under pathological conditions, Msx1 overexpression can cause cell dedifferentiation or cell apoptosis. We hypothesized that Msx1 overexpression contributes to loss of small pulmonary vessels in PAH. In IPAH lung, MSX1 protein localization was strikingly increased in muscularized remodeled pulmonary vessels, whereas it was undetectable in control pulmonary arteries. We developed a transgenic mouse model overexpressing MSX1 (MSX1
MeSH term(s)	Animals ; Apoptosis/physiology ; Cell Cycle/physiology ; Cell Differentiation/physiology ; Down-Regulation/physiology ; Female ; Humans ; Hypoxia/metabolism ; Lung/metabolism ; MSX1 Transcription Factor/metabolism ; Male ; Mice ; Pulmonary Artery/metabolism ; Up-Regulation/physiology
Chemical Substances	MSX1 Transcription Factor ; Msx1 protein, mouse
Language	English
Publishing date	2021-09-03
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10092306
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Article ; Online: Impact of Epicardial Adipose Tissue on Right Cardiac Function and Prognosis in Pulmonary Arterial Hypertension.

Chen, Yusi / Chen, Jingyuan / Li, Junli / Li, Fang / Chen, Zheng / Chen, Zhangling / Luo, Jun / Qiu, Haihua / Chen, Wenjie / Hu, Junjiao / Luo, Xiaoqin / Tan, Yingjie / Rathinasabapathy, Anandharajan / Li, Jiang

Chest

2023

Abstract: Background: Although epicardial adipose tissue (EAT) is linked to effects on survival in left-sided heart failure, the association between EAT and right-sided heart failure caused by pulmonary arterial hypertension (PAH) remains unknown.: Research ... ...

Abstract	Background: Although epicardial adipose tissue (EAT) is linked to effects on survival in left-sided heart failure, the association between EAT and right-sided heart failure caused by pulmonary arterial hypertension (PAH) remains unknown. Research question: What are the potential impacts of EAT volume (EATV) on right ventricular function, biomarkers of myocardial injury, and long-term prognosis in patients with PAH?. Study design and methods: A total of 135 age- and BMI-matched patients with PAH and 49 control subjects were included in this study. EATV was quantified by using cardiac magnetic resonance and was related to clinical correlates, N-terminal pro-brain natriuretic peptide, and cardiac function. Levels of EATV associated with the risk of clinical worsening were evaluated on a continuous scale (restricted cubic splines) and by previously defined centile categories with Cox proportional hazards regression models and Kaplan-Meier survival estimates. Results: Compared with the control subjects, patients with PAH had a lower EATV (ln [EATV], 3.2 ± 0.8 mL vs 3.5 ± 0.7 mL; P = .034). The association of EATV with right ventricular end-diastolic volume (P Interpretation: Patients with PAH had a decreased EATV compared with control subjects. EATV exhibited a U-shaped association with right ventricular function and biomarkers of myocardial injury in patients with PAH. Low and high levels of EATV might reduce long-term event-free survival in patients with PAH. Clinical trial registration: Chinese Clinical Trial Registry; No. ChiCTR2100049804; www.chictr.org.cn.
Language	English
Publishing date	2023-11-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	1032552-9
ISSN	1931-3543 ; 0012-3692
ISSN (online)	1931-3543
ISSN	0012-3692
DOI	10.1016/j.chest.2023.11.039
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Article ; Online: Overexpression of Msx1 in Mouse Lung Leads to Loss of Pulmonary Vessels Following Vascular Hypoxic Injury

James West / Anandharajan Rathinasabapathy / Xinping Chen / Sheila Shay / Shanti Gladson / Megha Talati

Cells, Vol 10, Iss 2306, p

2021 Volume 2306

Abstract	Pulmonary arterial hypertension (PAH) is a progressive lung disease caused by thickening of the pulmonary arterial wall and luminal obliteration of the small peripheral arteries leading to increase in vascular resistance which elevates pulmonary artery pressure that eventually causes right heart failure and death. We have previously shown that transcription factor Msx1 (mainly expressed during embryogenesis) is strongly upregulated in transformed lymphocytes obtained from PAH patients, especially IPAH. Under pathological conditions, Msx1 overexpression can cause cell dedifferentiation or cell apoptosis. We hypothesized that Msx1 overexpression contributes to loss of small pulmonary vessels in PAH. In IPAH lung, MSX1 protein localization was strikingly increased in muscularized remodeled pulmonary vessels, whereas it was undetectable in control pulmonary arteries. We developed a transgenic mouse model overexpressing MSX1 (MSX1 OE ) by about 4-fold and exposed these mice to normoxic, sugen hypoxic (3 weeks) or hyperoxic (100% 02 for 3 weeks) conditions. Under normoxic conditions, compared to controls, MSX1 OE mice demonstrated a 30-fold and 2-fold increase in lung Msx1 mRNA and protein expression, respectively. There was a significant retinal capillary dropout ( p < 0.01) in MSX1 OE mice, which was increased further ( p < 0.03) with sugen hypoxia. At baseline, the number of pulmonary vessels in MSX1 OE mice was similar to controls. In sugen-hypoxia-treated MSX1 OE mice, the number of small (0–25 uM) and medium (25–50 uM) size muscularized vessels increased approximately 2-fold ( p < 0.01) compared to baseline controls; however, they were strikingly lower ( p < 0.001) in number than in sugen-hypoxia-treated control mice. In MSX1 OE mouse lung, 104 genes were upregulated and 67 genes were downregulated compared to controls. Similarly, in PVECs, 156 genes were upregulated and 320 genes were downregulated from siRNA to MSX1 OE , and in PVSMCs, 65 genes were upregulated and 321 genes were downregulated from ...
Keywords	pulmonary arterial hypertension ; Msx1 expression ; mouse models ; pulmonary vascular endothelial cells ; pulmonary vascular smooth muscle cells ; BMP pathway ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2021-09-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Differential serum lipid distribution in IPAH and CHD-PAH patients.

Chen, Jingyuan / Rathinasabapathy, Anandharajan / Luo, Jun / Yang, Xiaojie / Luo, Peng / Chen, Yusi / Li, Zilu / Li, Jiang

Respiratory medicine

2021 Volume 191, Page(s) 106711

Abstract: Lipid homeostasis is dysregulated in pulmonary arterial hypertension (PAH). A decrease in serum high- and low-density lipoprotein cholesterol (HDL-C and LDL-C) is significantly associated with the worse prognosis of PAH. However, no study has ... ...

Abstract	Lipid homeostasis is dysregulated in pulmonary arterial hypertension (PAH). A decrease in serum high- and low-density lipoprotein cholesterol (HDL-C and LDL-C) is significantly associated with the worse prognosis of PAH. However, no study has investigated the differential distribution of lipids in various PAH subtypes. We enrolled 190 patients in this retrospective study, which includes 20 patients with congenital heart disease without PAH (CHD-nonPAH), 101 patients with PAH associated with congenital heart disease (CHD-PAH), 69 patients with idiopathic PAH (IPAH) and 81 healthy controls. Laboratory parameters such as liver and renal function, serum lipids, C-reactive protein, N-terminal pro-brain natriuretic peptide (NT-proBNP), echocardiography, right heart catheterization and 6-min walk distance (6MWD) were performed. All types of cholesterol including HDL-C, LDL-C and total cholesterol (CHOL) were significantly lower in IPAH patients in association with right heart function. Although LDL-C and CHOL were lower in CHD-PAH, they were not associated with disease severity or heart failure. Thus, we conclude that IPAH and CHD-PAH patients exhibited a differential distribution pattern of serum lipids.
MeSH term(s)	Familial Primary Pulmonary Hypertension/complications ; Humans ; Hypertension, Pulmonary ; Lipids ; Pulmonary Arterial Hypertension ; Retrospective Studies
Chemical Substances	Lipids
Language	English
Publishing date	2021-12-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1003348-8
ISSN	1532-3064 ; 0954-6111
ISSN (online)	1532-3064
ISSN	0954-6111
DOI	10.1016/j.rmed.2021.106711
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Article ; Online: Association of cardiac injury with hypertension in hospitalized patients with COVID-19 in China.

Zeng, Xiaofang / Rathinasabapathy, Anandharajan / Liu, Dongliang / Zha, Lihuang / Liu, Xiangwei / Tang, Yiyang / Li, Famei / Lin, Wenchao / Yu, Zaixin / Chen, Huiling

Scientific reports

2021 Volume 11, Issue 1, Page(s) 22389

Abstract: Outbreak of global pandemic Coronavirus disease 2019 (COVID-19) has so far caused countless morbidity and mortality. However, a detailed report on the impact of COVID-19 on hypertension (HTN) and ensuing cardiac injury is unknown. Herein, we have ... ...

Abstract	Outbreak of global pandemic Coronavirus disease 2019 (COVID-19) has so far caused countless morbidity and mortality. However, a detailed report on the impact of COVID-19 on hypertension (HTN) and ensuing cardiac injury is unknown. Herein, we have evaluated the association between HTN and cardiac injury in 388 COVID-19 (47.5 ± 15.2 years) including 75 HTN and 313 normotension. Demographic data, cardiac injury markers, other laboratory findings, and comorbidity details were collected and analyzed. Compared to patients without HTN, hypertensive-COVID-19 patients were older, exhibited higher C-reactive protein (CRP), erythrocyte sedimentation rate, and comorbidities such as diabetes, coronary heart disease, cerebrovascular disease and chronic kidney disease. Further, these hypertensive-COVID-19 patients presented more severe disease with longer hospitalization time, and a concomitant higher rate of bilateral pneumonia, electrolyte disorder, hypoproteinemia and acute respiratory distress syndrome. In addition, cardiac injury markers such as creatine kinase (CK), myoglobin, lactic dehydrogenase (LDH), and N-terminal pro brain natriuretic peptide were significantly increased in these patients. Correlation analysis revealed that systolic blood pressure correlated significantly with the levels of CK, and LDH. Further, HTN was associated with increased LDH and CK-MB in COVID- 19 after adjusting essential variables. We also noticed that patients with elevated either high sensitivity-CRP or CRP demonstrated a significant high level of LDH along with a moderate increase in CK (p = 0.07) and CK-MB (p = 0.09). Our investigation suggested that hypertensive patients presented higher risk of cardiac injury and severe disease phenotype in COVID-19, effectively control blood pressure in HTN patients might improve the prognosis of COVID-19 patients.
MeSH term(s)	Adult ; Biomarkers/blood ; COVID-19/complications ; China/epidemiology ; Comorbidity ; Disease Outbreaks ; Female ; Heart Diseases/epidemiology ; Heart Injuries/epidemiology ; Hospitalization ; Humans ; Hypertension/epidemiology ; Male ; Middle Aged ; Prognosis ; SARS-CoV-2/pathogenicity
Chemical Substances	Biomarkers
Language	English
Publishing date	2021-11-17
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-01796-0
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Article ; Online: Association of cardiac injury with hypertension in hospitalized patients with COVID-19 in China

Xiaofang Zeng / Anandharajan Rathinasabapathy / Dongliang Liu / Lihuang Zha / Xiangwei Liu / Yiyang Tang / Famei Li / Wenchao Lin / Zaixin Yu / Huiling Chen

Scientific Reports, Vol 11, Iss 1, Pp 1-

2021 Volume 10

Abstract: Abstract Outbreak of global pandemic Coronavirus disease 2019 (COVID-19) has so far caused countless morbidity and mortality. However, a detailed report on the impact of COVID-19 on hypertension (HTN) and ensuing cardiac injury is unknown. Herein, we ... ...

Abstract	Abstract Outbreak of global pandemic Coronavirus disease 2019 (COVID-19) has so far caused countless morbidity and mortality. However, a detailed report on the impact of COVID-19 on hypertension (HTN) and ensuing cardiac injury is unknown. Herein, we have evaluated the association between HTN and cardiac injury in 388 COVID-19 (47.5 ± 15.2 years) including 75 HTN and 313 normotension. Demographic data, cardiac injury markers, other laboratory findings, and comorbidity details were collected and analyzed. Compared to patients without HTN, hypertensive-COVID-19 patients were older, exhibited higher C-reactive protein (CRP), erythrocyte sedimentation rate, and comorbidities such as diabetes, coronary heart disease, cerebrovascular disease and chronic kidney disease. Further, these hypertensive-COVID-19 patients presented more severe disease with longer hospitalization time, and a concomitant higher rate of bilateral pneumonia, electrolyte disorder, hypoproteinemia and acute respiratory distress syndrome. In addition, cardiac injury markers such as creatine kinase (CK), myoglobin, lactic dehydrogenase (LDH), and N-terminal pro brain natriuretic peptide were significantly increased in these patients. Correlation analysis revealed that systolic blood pressure correlated significantly with the levels of CK, and LDH. Further, HTN was associated with increased LDH and CK-MB in COVID- 19 after adjusting essential variables. We also noticed that patients with elevated either high sensitivity-CRP or CRP demonstrated a significant high level of LDH along with a moderate increase in CK (p = 0.07) and CK-MB (p = 0.09). Our investigation suggested that hypertensive patients presented higher risk of cardiac injury and severe disease phenotype in COVID-19, effectively control blood pressure in HTN patients might improve the prognosis of COVID-19 patients.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2021-11-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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