PM2.5 exposure aggravates left heart failure induced pulmonary hypertension

Chen, Jun-Jiang; Ma, Wenqi; Yuan, Jingliang; Cui, Lianqun

doi:10.1080/00015385.2018.1488568

Cited by 18 publications

(8 citation statements)

References 23 publications

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“…Another common model for pressure‐load‐induced HF in mice is TAC. In 1991, Rockman et al 44 first applied this model to the study of cardiomyocyte hypertrophy in mice by the ligation of transverse aorta using a 27 G blunt needle positioned between the innominate artery and the left carotid artery, which over a 6‐week period established a mouse PH model caused by left HF with medium hemodynamic compromise (RVSP 35–40 mmHg) 45,46 . After TAC in mice, left ventricular insufficiency, right ventricular hypertrophy, increased RVSP, and elevated mPAP develop over time, accompanied by an increased degree of pulmonary fibrosis and infiltration of inflammatory cells 47 .…”

Section: Ph From Pressure Overload‐induced Left‐ventricular (Lv) Failurementioning

confidence: 99%

Animal models of pulmonary hypertension due to left heart disease

Liu

2022

Anim Models and Exp Med

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Pulmonary hypertension (PH) is a progressive cardiovascular disorder of multiple etiologies that typically ends in death due to right heart failure (HF). Based on the World Health Organization (WHO) classification of PH, it is divided into 5 groups, of which PH due to left heart disease (PH-LHD) is the commonest. PH-LHD is described as a PH subtype with mean pulmonary artery pressure (mPAP) >25 mmHg and pulmonary artery wedge pressure (PAWP) >15 mmHg, 1 although the threshold values of PAWP are controversial. 2 HF caused by LHD is mainly manifested as reduced ejection fraction (HFrEF), with preserved ejection fraction (HFpEF) and leftsided heart valve disease (VHD). 3 The occurrence of PH in patients with LHD is a sign of disease progression. 4 Nevertheless, therapeutic agents directly targeting patients with PH-LHD are not available.Although there have been some studies supporting the treatment of PH-LHD with targeted drugs for PAH, none has been applied to clinical treatment of PH-LHD. [5][6][7][8][9][10][11][12][13][14][15][16] Effective treatments for LHD do not seem to improve PH-LHD, 17 because PH-LHD is divided hemodynamically into pure postcapillary PH and combined pre-and

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Section: Ph From Pressure Overload‐induced Left‐ventricular (Lv) Failurementioning

confidence: 99%

Animal models of pulmonary hypertension due to left heart disease

Liu

2022

Anim Models and Exp Med

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“…Pulmonary fibrosis is characterized by the deposition of collagen and other extracellular matrix molecules. 20 In a recent study, Chen et al 21 observed that PM2.5 increased the expression of TGF-β and collagen III deposition, which was responsible for right ventricle and pulmonary fibrosis. As was known to us, some particles in air such as PM2.5 were related to a lot of chronic respiratory diseases caused by pulmonary inflammation and fibrosis.…”

Section: Discussionmentioning

confidence: 98%

“…In a latest report, male Wistar rats model with local exposure to PM2.5 was built successfully. 21 In this study, PM2.5 particles in the real atmosphere were collected by PM2.5 detection equipment of Binhai New Area Environmental Monitoring Station in Tianjin. Wistar rats were dripped saline and different concentration of PM2.5 suspension solution and killed after 6 weeks.…”

Section: Discussionmentioning

confidence: 99%

PM2.5 inducing myocardial fibrosis mediated by Ang II/ERK1/2/TGF-β₁ signaling pathway in mice model

Zang

Zhao

2021

J Renin Angiotensin Aldosterone Syst

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Objects: To discuss the influence of PM2.5 on myocardial fibrosis and related mechanism. Methods: PM2.5 particles were prepared into different concentrations of solution to drip into the mice’s trachea twice each week. The mice were divided into five groups, Blank control group (C group), NS control group (J group), high dose group (G group, 10 mg/kg), medium dose group (Z group, 5 mg/kg), and 1ow dose group (D group, 2.5 mg/kg). After 6 weeks, the myocardial fibrosis was observed by HE and Masson staining. The expression of Ang II, ERK1/2, and TGF-β1 was examined by Western Blotting (WB) and Real time PCR (RT-PCR). Results: The higher dose PM2.5 was administrated, the worse the myocardial fibrosis was in PM2.5 groups. The expression of Ang II, ERK1/2, and TGF-β1 was increased in higher dose groups in protein and mRNA level. Conclusion: 1. PM2.5 induced the cardiac fibrosis. 2. PM2.5 dripped into trachea in mice model activated the expression of Ang II, ERK1/2, and TGF-β1. The activation of renin-angiotensin system (RAS) was suggested to participate in the cardiac fibrosis induced by PM2.5.

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“…PM2.5 is one of the major pollutants during our daily life. PM2.5 exposure can aggravate and induce PH disease [ 63 ]. Mouse chronic exposure to PM2.5 induced the EndMT process in the lung tissues.…”

Section: Long Noncoding Rnas (Lncrnas) In Pulmonary Hypertensionmentioning

confidence: 99%

The Landscape of Noncoding RNA in Pulmonary Hypertension

et al. 2022

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The transcriptome of pulmonary hypertension (PH) is complex and highly genetically heterogeneous, with noncoding RNA transcripts playing crucial roles. The majority of RNAs in the noncoding transcriptome are long noncoding RNAs (lncRNAs) with less circular RNAs (circRNAs), which are two characteristics gaining increasing attention in the forefront of RNA research field. These noncoding transcripts (especially lncRNAs and circRNAs) exert important regulatory functions in PH and emerge as potential disease biomarkers and therapeutic targets. Recent technological advancements have established great momentum for discovery and functional characterization of ncRNAs, which include broad transcriptome sequencing such as bulk RNA-sequence, single-cell and spatial transcriptomics, and RNA-protein/RNA interactions. In this review, we summarize the current research on the classification, biogenesis, and the biological functions and molecular mechanisms of these noncoding RNAs (ncRNAs) involved in the pulmonary vascular remodeling in PH. Furthermore, we highlight the utility and challenges of using these ncRNAs as biomarkers and therapeutics in PH.

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PM2.5 exposure aggravates left heart failure induced pulmonary hypertension

Cited by 18 publications

References 23 publications

Animal models of pulmonary hypertension due to left heart disease

Animal models of pulmonary hypertension due to left heart disease

PM2.5 inducing myocardial fibrosis mediated by Ang II/ERK1/2/TGF-β₁ signaling pathway in mice model

The Landscape of Noncoding RNA in Pulmonary Hypertension

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PM2.5 exposure aggravates left heart failure induced pulmonary hypertension

Cited by 18 publications

References 23 publications

Animal models of pulmonary hypertension due to left heart disease

Animal models of pulmonary hypertension due to left heart disease

PM2.5 inducing myocardial fibrosis mediated by Ang II/ERK1/2/TGF-β1 signaling pathway in mice model

The Landscape of Noncoding RNA in Pulmonary Hypertension

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PM2.5 inducing myocardial fibrosis mediated by Ang II/ERK1/2/TGF-β₁ signaling pathway in mice model