AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY美国呼吸细胞与分子生物学杂志
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY(英文缩写 AM J RESP CELL MOL),ISSN 1044-1549,eISSN 1535-4989,中文译名:美国呼吸细胞与分子生物学杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-10-01 至 2026-09-30，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 7.748 | Q1 |
| 2022 | 6.400 | Q1 |
| 2023 | 5.900 | Q1 |
| 2024 | 5.300 | Q1 |
| 2025 | 5.400 | Q1 |
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY 最新收录文献
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1. Role of carbonic anhydrases 9 and 12 in hypoxia and non-hypoxia associated pulmonary hypertension.
PMID:日期:2026-09-30Pulmonary hypertension (PH) is characterized by several cancer-like attributes, such as dysregulated proliferation and migration of pulmonary vascular cells. Carbonic anhydrases (CA)9 and 12 are elevated in various types of tumor tissues and play a major role in the pH regulation system of cancer cells. CA9 and 12 engagement in the pathology of PH remains unclear. Lung tissue samples from PH patients were analyzed for CA9 and 12 expression profiles. Circulating CA9 levels were measured in the plasma of PH patients and Kyrgyz highlanders. In vitro expression and functional studies were conducted in pulmonary arterial smooth muscle cells (PASMCs). Finally, two in vivo studies were carried out to investigate the therapeutic potential of the specific CA9 and 12 inhibitor S4. The mRNA and protein expression of CA9 and 12 were upregulated in lungs of PH patients and during hypoxic and non-hypoxic stimulation of PASMCs. Circulating CA9 levels were elevated in both PH patients and Kyrgyz highlanders with PH. Furthermore, CA9 and 12 played an important role in the proliferation and migration of PASMCs. Our study demonstrated that CA9 and 12 are crucial for maintaining pH homeostasis in PASMCs and, subsequently, for the activation of protein kinases. Finally, pharmacological inhibition of CA9 and 12 ameliorated the development of monocrotaline-induced PH in rats and chronic hypoxia-induced PH in mice. Our study provides evidence that CA9 and 12 are engaged in the pathogenesis of hypoxia and non-hypoxia associated PH and may represent novel therapeutic targets in future.
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2. E‑Cigarette Aerosols Trigger Mitochondrial Dysfunction-Associated Ferroptosis in Human Primary ATII Cells.
PMID:日期:2026-09-25E‑cigarettes contain nicotine and flavoring compounds. They can disrupt mitochondrial homeostasis, injure the alveolar epithelium, and ultimately contribute to lung dysfunction. To investigate the systemic response, plasma was obtained from e-cigarette users. Mitochondrial DNA damage was detected, suggesting that vaping alters cell physiology. ATII cells are highly abundant in mitochondria and dependent on their integrity for surfactant production and alveolar epithelial regeneration. ATII cells and PCLS were obtained from organ donors to examine the effects of cinnamon roll-flavored e-cigarette aerosols with nicotine. E-cigarette aerosols induced mitochondrial DNA damage and lipid peroxidation, as indicated by elevated MitoCLox levels. Additionally, reduced levels of mitochondrial respiratory chain subunits NDUFS1 and UQCRC2 were detected in ATII cells, suggesting disruption of complexes I and III, respectively. A similar decrease was observed in ATII cells in wild-type mice after treatment with cinnamon roll-flavored e-cigarette aerosols with nicotine. Furthermore, increased LAMP2 and LC3B levels were found, indicating autophagy. This response was accompanied by decreased GPX4 and increased ACSL4 protein expression, a molecular signature characteristic of ferroptosis. The role of DJ-1 was analyzed following this exposure, as it is localized in mitochondria. ATII cells in DJ-1 KO mice had reduced SP-C expression. Also, DJ-1 deficiency in cells led to increased mitochondrial superoxide production, suggesting a cytoprotective function for DJ-1. These findings demonstrate that cinnamon roll-flavored e-cigarette aerosols with nicotine disrupt mitochondrial function, alter cytosol-mitochondria crosstalk, and induce ATII cell ferroptosis as a mechanism of vaping-associated lung injury.
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5. Pathological Th2 cell activation via STAT6 pathway for pulmonary fibrosis.
PMID:日期:2026-09-16Idiopathic pulmonary fibrosis is a progressive and fatal lung disease in which type 2 immunity has been implicated, yet the upstream signals that sustain pathogenic T helper 2 (Th2) programs and coordinate immune-stromal remodeling remain incompletely defined. We integrated single-cell RNA sequencing from human fibrotic lungs with complementary mechanistic studies in the bleomycin mouse model to test whether CD28 costimulation engages JAK1/STAT6 signaling to drive fibrogenic inflammation. Transcriptomic analyses identified expansion of Th2 cells with elevated CD28 expression and increased STAT6 pathway activity in human IPF and bleomycin-injured mouse lungs, accompanied by transcriptional programs consistent with profibrotic monocyte-derived alveolar macrophages and activated fibroblasts. To establish causality and therapeutic relevance, we perturbed this axis in vivo after injury initiation. Antibody-mediated CD28 blockade, pharmacologic STAT6 inhibition, and genetic STAT6 deficiency each reduced Th2 accumulation and monocyte-derived alveolar macrophages, diminished collagen deposition and histologic fibrosis, and improved lung mechanics. Conversely, agonistic CD28 engagement amplified Th2 and myeloid profibrotic responses, increased collagen accumulation, and worsened pulmonary function. Across species and interventions, changes in Th2-associated signaling tracked with downstream profibrotic myeloid and stromal programs, supporting a coordinated circuit linking adaptive costimulation to fibrotic remodeling. These findings define a CD28-JAK1/STAT6-Th2-monocyte-derived alveolar macrophage pathway as a mechanistic driver of pulmonary fibrosis and nominate CD28 and STAT6 as actionable immunologic targets that could complement existing antifibrotic therapies.
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8. Mechanical Ventilation During Neonatal Hyperoxia Causes Thrombospondin-1 Dependent Lung Remodeling in Mice.
PMID:日期:2026-09-15Extremely premature infants are simultaneously exposed to hyperoxia (O2) and mechanical ventilation (MV) as a life-saving intervention, but these stimuli increase their risk of developing Bronchopulmonary Dysplasia (BPD). Passive O2 models have traditionally been used to model BPD, however, these models do not account for superimposed mechanical stretch responses in the developing lung. To address this gap, we engineered a novel, non-invasive rodent model of combined O2-MV wherein mice are exposed to cyclic positive pressure with either room air (RA) or hyperoxia (100% O2) for 6 hours per day from postnatal days (PND) 1-4 and then recovered in room air. Pulmonary function testing revealed that O2-control mice had decreased resistance and increased compliance, consistent with expected findings in a distensible, simplified lung. In contrast, function studies in O2-MV mice were partially normalized, with persistent remodeling of collagen and elastin fiber networks and less alveolar simplification than O2-controls. Transcriptomic analyses at PND4 revealed several extracellular matrix (ECM) genes induced by combined O2-MV, including glycoprotein Thrombospondin-1 (Thbs1), confirmed by immunohistochemistry and qRT-PCR. To test the contribution of Thbs1 to lung remodeling, exposure of neonatal Thbs1 -/- mice to O2-MV led to growth failure, alveolar simplification, and reversal of lung function and collagen remodeling changes at PND 28, suggesting that O2-MV remodels the lung collagen fiber networks through Thbs1 expression. Our findings establish a mechanistic link between Thbs1 and ECM remodeling and emphasize the need to better understand how MV in the setting of neonatal hyperoxia contributes to the pathogenesis of BPD.
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9. Interrogation of functional variants in COPD GWAS loci by massively parallel reporter assays.
PMID:日期:2026-09-15Genome-wide association study (GWAS) loci often contain many linked variants, making it difficult to determine which variant is functionally relevant. Massively parallel reporter assays (MPRA) allow experimental testing of candidate variants to identify those with regulatory activity. Prior chronic obstructive pulmonary disease (COPD) MPRA studies have largely focused on individual loci, whereas broader multi-locus, multi-cell-type interrogation remains limited. We aim to identify functional variants in five COPD GWAS loci across three lung-relevant cell types. We screened 1120 variants using MPRA in epithelial (16HBE), fibroblast (MRC5), and endothelial (HUVEC) cells followed by reporter assay validation. Public Hi-C, ChIP-seq and ATAC-seq datasets were analyzed to evaluate chromatin context near candidate variants. We further performed CRISPR interference (CRISPRi) targeting variant-containing regions and measured gene expression by RT-qPCR in primary normal human bronchial epithelial (NHBE) cells using two gRNAs per variant. Co-immunoprecipitation was performed to test interaction between selected candidate genes. In MPRA, we identified 25 variants with allele-specific effects (∼2% of tested variants). Enrichment of H3K27Ac and open chromatin near rs35421223 was detected in 16HBE cells. CRISPRi identified two SNP-gene pairs, RUVBL1 and RAB7A regulated by rs35421223 in both the 16HBE cell line and primary NHBE cells. We detected interaction between RUVBL1 and the known COPD gene product FAM13A. Screening COPD loci across three cell types identified functional regulatory variants and linked them to candidate target genes for future mechanistic studies.