Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (598 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Damage to any compartment of the lung caused by physical, chemical, or biological agents which characteristically elicit inflammatory reaction. These inflammatory reactions can either be acute and dominated by neutrophils, or chronic and dominated by lymphocytes and macrophages.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Injuries, Lung; Injury, Lung; Lung Injuries; Pulmonary Injury; Injuries, Pulmonary; Injury, Pulmonary; Pulmonary Injuries; Chronic Lung Injury.
Where it fits in the MeSH classification
- Broader topics
- Lung Diseases; Thoracic Injuries
- Narrower topics
- Acute Lung Injury; Meconium Aspiration Syndrome; Pneumoconiosis; Radiation Pneumonitis; Ventilator-Induced Lung Injury
Related concepts
Research landscape
PubMed indexes 54,329 records tagged with the MeSH heading “Lung Injury” (counts retrieved 2026-11-04). 13,206 of them (24.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 19,415 records.
Reviews account for 5,840 records (10.7%) and meta-analyses for 468. Randomized controlled trials number 924 (1.7%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 19,415 |
| 2000-2009 | 6,370 |
| 2010-2019 | 15,338 |
| 2020 onward | 13,206 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 5,840 | 10.7% |
| Meta-analyses | 468 | 0.9% |
| Randomized controlled trials | 924 | 1.7% |
Method: PubMed query "Lung Injury"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in respiratory medicine
Research on airway and lung disease mixes lung-function tests, symptom diaries, imaging and hospital records, so what was measured and in whom matters as much as the result. Many conditions here, such as asthma and COPD, vary between people and over time, and exposure studies (smoking, pollution, workplace dust) show association rather than proof of cause. Nothing on this page is advice about treatment or inhalers; anyone with breathing difficulty should seek care from a qualified clinician. Check how the condition was defined, the severity of the people studied and whether outcomes were symptoms, lung function or hospital admissions.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| NINJ1 plays a vital role in the release of neutrophil extracellular traps during acute lung injury | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42350381 · DOI · PMC13558649 |
| Perturbation of the preterm human immune system in early life | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42013158 · DOI · PMC13313540 |
| Targeting mitochondrial apoptosis in septic lung injury: protective potential of omega-3 fatty acids | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41894027 · DOI · PMC13031218 |
NINJ1 plays a vital role in the release of neutrophil extracellular traps during acute lung injury [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Excessive neutrophil extracellular traps (NETs) formation is a significant contributor to acute lung injury (ALI), making its inhibition a novel therapeutic avenue to improve outcomes.
- Closing excerpt
- K45 and N60 are essential for NINJ1 oligomerization and subsequent NET release.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (169 words)
Excessive neutrophil extracellular traps (NETs) formation is a significant contributor to acute lung injury (ALI), making its inhibition a novel therapeutic avenue to improve outcomes. In this study, we revealed that a novel pore-forming protein ninjurin-1 (NINJ1) was highly expressed in pro-inflammatory neutrophil subpopulations during ALI, using public single-cell RNA sequencing and hotspot analysis. Furthermore, we demonstrated that the NINJ1 oligomerization was essential for the NET release in neutrophils from both acute respiratory distress syndrome (ARDS) patients and ALI mice. Genetic ablation of Ninj1 in neutrophils abolished NET release, thereby attenuating pulmonary dysfunction and reducing ALI-related lethality. Mechanistically, we found that K45 and N60 are critical for NINJ1 oligomerization and subsequent NET release. In summary, our findings reveal a novel pore-forming protein-mediated mechanism for NET release and highlight NINJ1 as a potential therapeutic target for the treatment of ALI/ARDS. Schematic illustration. The novel pore-forming protein NINJ1 mediates the extrusion of NETs, thereby exacerbating pulmonary injury in ARDS/ALI. K45 and N60 are essential for NINJ1 oligomerization and subsequent NET release.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42350381 · DOI · PMC13558649
Perturbation of the preterm human immune system in early life [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Although inflammatory complications are common in preterm infants, the effects of these conditions on neonatal immune development remain poorly defined.
- Closing excerpt
- Thus, comprehensive and longitudinal immune profiling may not only identify connections between clinical inflammatory complications and underlying immune pathways but also reveal potential targets for intervention.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (175 words)
Although inflammatory complications are common in preterm infants, the effects of these conditions on neonatal immune development remain poorly defined. We therefore investigated whether severe bronchopulmonary dysplasia (BPD) and systemic infection, 2 major complications of prematurity, produce distinct immune signatures and change immune composition over time. We performed longitudinal high-dimensional immune profiling of residual whole blood from 38 preterm infants sampled every 2 weeks, along with 10 term infants at birth. Preterm infants with severe BPD showed a progressive increase in Th17-polarized CD4+ T cells, neutrophils, and Th17-related cytokines compared with age-matched infants with moderate BPD. In contrast, some preterm infants with systemic bacterial or viral infections mounted exceptionally robust CD8+, CD4+, and γδ T cell responses, with oligoclonal expansion, terminal differentiation, and coordinated plasma cytokine shifts that persisted well beyond resolution of infection. These findings demonstrate that different preterm comorbidities imprint the neonatal immune system in divergent ways. Thus, comprehensive and longitudinal immune profiling may not only identify connections between clinical inflammatory complications and underlying immune pathways but also reveal potential targets for intervention.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42013158 · DOI · PMC13313540
Targeting mitochondrial apoptosis in septic lung injury: protective potential of omega-3 fatty acids [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Acute lung injury secondary to sepsis remains a major problem in critical patients.
- Closing excerpt
- These findings highlight the therapeutic potential of OM3 in mitigating sepsis-associated pulmonary damage through mitochondrial preservation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (254 words)
Acute lung injury secondary to sepsis remains a major problem in critical patients. Lipopolysaccharide (LPS)-induced lung injury is characterized by inflammatory infiltration, oxidative stress, and extensive apoptosis, particularly via the mitochondrial pathway. Omega-3 (OM3) polyunsaturated fatty acids have been proposed as promising modulators of inflammation and oxidative damage. However, their role in regulating mitochondria-mediated apoptosis in sepsis remains underexplored. Thirty-two female Wistar albino rats were randomized into four groups: Control, LPS (5 mg/kg, i.p. 3th), LPS-OM3 (400 mg/kg/day, i.p., 3 day), and OM3 only. After 72 h, lung tissues were collected for histopathological scoring, immunohistochemistry as tumor necrosis factor-alpha (TNF-α), heat shock protein (HSP70), caspase-3 (Cas-3); biochemical analyses as total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI) and qRT-PCR for mitochondrial apoptosis markers B cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), cytochrome-c (Cyt-c) and Cas-9. LPS induced ALI characterized by bronchiolar epithelial degeneration, alveolar hemorrhage, inflammation, and hyaline membrane formation. Biochemically, TOS and OSI levels were significantly elevated, while TAS remained unchanged. Immunohistochemical and genetic analysis showed marked upregulation of TNF-α, HSP70, and Cas-3 Bax, Cyt-c, and Casp-9 expression and decreased Bcl-2 expression in the LPS group. OM3 supplementation significantly attenuated histopathological damage, reduced oxidative stress markers, suppressed immunopositivity of proinflammatory and apoptotic proteins, and favorably modulated the apoptosis-related gene expressions. OM3 fatty acids exert a potent protective effect against LPS-induced ALI by suppressing mitochondrial apoptosis, reducing oxidative stress, and modulating the inflammatory response. These findings highlight the therapeutic potential of OM3 in mitigating sepsis-associated pulmonary damage through mitochondrial preservation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41894027 · DOI · PMC13031218
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis [4]
- Research article Radiation dose-volume effects in the lung [5]
- Research article Non-invasive versus invasive respiratory support in preterm infants at birth: systematic review and meta-analysis [6]
- Research article Meta-analysis: ventilation strategies and outcomes of the acute respiratory distress syndrome and acute lung injury [7]
- Research article Use of corticosteroids in acute lung injury and acute respiratory distress syndrome: a systematic review and meta-analysis [8]
- Research article Recruitment maneuvers for acute lung injury: a systematic review [9]
References
- Zhong WJ, Liu YB, Yang XY, Chen MR, Yang NS, Zhang CY, et al.. NINJ1 plays a vital role in the release of neutrophil extracellular traps during acute lung injury. . 2026. PMID 42350381 · DOI · PMC13558649
- Fensterheim BA, McKeague ML, Mathew D, Shwetank S, Pattekar A, Lee M, et al.. Perturbation of the preterm human immune system in early life. . 2026. PMID 42013158 · DOI · PMC13313540
- Çelik E, Karabacak P, Özcan MS, İlhan İ, Tepebaşı MY, Sarman E, et al.. Targeting mitochondrial apoptosis in septic lung injury: protective potential of omega-3 fatty acids. . 2026. PMID 41894027 · DOI · PMC13031218
- Briel M, Meade M, Mercat A, Brower RG, Talmor D, Walter SD, et al.. Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis. JAMA. 2010. PMID 20197533 · DOI
- Marks LB, Bentzen SM, Deasy JO, Kong FM, Bradley JD, Vogelius IS, et al.. Radiation dose-volume effects in the lung. Int J Radiat Oncol Biol Phys. 2010. PMID 20171521 · DOI · PMC3576042
- Schmölzer GM, Kumar M, Pichler G, Aziz K, O'Reilly M, Cheung PY. Non-invasive versus invasive respiratory support in preterm infants at birth: systematic review and meta-analysis. BMJ. 2013. PMID 24136633 · DOI · PMC3805496
- Putensen C, Theuerkauf N, Zinserling J, Wrigge H, Pelosi P. Meta-analysis: ventilation strategies and outcomes of the acute respiratory distress syndrome and acute lung injury. Ann Intern Med. 2009. PMID 19841457 · DOI
- Tang BM, Craig JC, Eslick GD, Seppelt I, McLean AS. Use of corticosteroids in acute lung injury and acute respiratory distress syndrome: a systematic review and meta-analysis. Crit Care Med. 2009. PMID 19325471 · DOI
- Fan E, Wilcox ME, Brower RG, Stewart TE, Mehta S, Lapinsky SE, et al.. Recruitment maneuvers for acute lung injury: a systematic review. Am J Respir Crit Care Med. 2008. PMID 18776154 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.