ReviewMolecular and cellular biochemistry2021
Involvement of 4-hydroxy-2-nonenal in the pathogenesis of pulmonary fibrosis.
Review in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 26 citations in OpenAlex.
- Arsenic Inhibits the PA28α/β-PSMB5 Pathway Blocking Phosphorylated TFEB Degradation and Causing Lysosomal Dysfunction that Damages the Liver.Biological trace element research · 2026Article
- 4-Hydroxynonenal, a Potential Biomarker for Lung Inflammatory Diseases.International journal of molecular sciences · 2026Review
- Progress in the Cross-Organ Biomarker oxLDL in Promoting Pathological Neovascular Diseases.Antioxidants (Basel, Switzerland) · 2026Review
- Genkwanin alleviates paraquat-induced acute lung injury by activating SIRT1-mediated Nrf2/HO-1 signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The interplay of ferroptosis and oxidative stress in pulmonary fibrosis: from mechanisms to treatment.Frontiers in cell and developmental biology · 2026Review
- The Redox-Adhesion-Exosome (RAX) Hub in Cancer: Lipid Peroxidation-Driven EMT Plasticity and Ferroptosis Defense with HNE/MDA Signaling and Lipidomic Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
- Unveiling the therapeutic mechanisms of Saorilao-4 decoction in pulmonary fibrosis through metabolomics and transcriptomics.Frontiers in nutrition · 2025Article
- Oxidative stress products and managements in atopic dermatitis.Frontiers in medicine · 2025Review
- Emerging roles of ferroptosis in pulmonary fibrosis: current perspectives, opportunities and challenges.Cell death discovery · 2024Review
- Under the dual effect of inflammation and pulmonary fibrosis, CTD-ILD patients possess a greater susceptibility to VTE.Thrombosis journal · 2024Review
- Dihydroartemisinin (DHA) inhibits myofibroblast differentiation through inducing ferroptosis mediated by ferritinophagy.Heliyon · 2024Article
- Epithelial-mesenchymal interaction protects normal colonocytes from 4-HNE-induced phenotypic transformation.PloS one · 2024Article
- Ferrostatin-1 attenuates hypoxic-ischemic brain damage in neonatal rats by inhibiting ferroptosis.Translational pediatrics · 2023Article
- Oxidative Stress in Health and Disease.Biomedicines · 2023Review
- Article
- Novel PD-L1-Targeted Phenyl-Pyrazolone Derivatives with Antioxidant Properties.Molecules (Basel, Switzerland) · 2023Article
- Correlation between serum 4-HNE and lactic acid levels and disease status in patients with severe pneumonia and its diagnostic value and prognostic evaluation.American journal of translational research · 2023Article
- NOX4 inhibition promotes the remodeling of dystrophic muscle.JCI insight · 2022Article
- 3'UTR shortening of profibrotic genes and reversibility of fibrosis in patients with end-stage right ventricular failure.Clinical and translational medicine · 2022Article
- 3'5-Dimaleamylbenzoic Acid Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Pulmonary fibrosis is a chronic progressive disease with high incidence, prevalence, and mortality rates worldwide. It is characterized by excessive accumulation of extracellular matrix in the lung parenchyma. The cellular and molecular mechanisms involved in its pathogenesis are complex, and some are still unknown. Several studies indicate that oxidative stress, characterized by overproduction of 4-hydroxy-2-nonenal (4-HNE), is an important player in pulmonary fibrosis. 4-HNE is a highly reactive compound derived from polyunsaturated fatty acids that can react with proteins, phospholipids, and nucleic acids. Thus, many of the altered cellular mechanisms that contribute to this disease can be explained by the participation of 4-HNE. Here, we summarize the current knowledge on the molecular states and signal transduction pathways that contribute to the pathogenesis of pulmonary fibrosis. Furthermore, we describe the participation of 4-HNE in various mechanisms involved in pulmonary fibrosis development, with a focus on the cell populations involved in the initiation, development, and maintenance of the fibrotic process, mainly alveolar cells, endothelial cells, macrophages, and inflammatory cells. Due to its characteristic activity as a second messenger, 4-HNE, in addition to being a consequence of oxidative stress, can support maintenance of the inflammatory and fibrotic process by spreading the effects of reactive oxygen species (ROS). Thus, regulation of 4-HNE levels could be a viable strategy to reduce its effects on the mechanisms involved in pulmonary fibrosis development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.