Related Experiment Video
Updated: Apr 24, 2026
04:45
Mouse Model of Oleic Acid-Induced Acute Respiratory Distress Syndrome
Published on: June 2, 2022
2.5K
Integrated Bioinformatic Identification and Experimental Validation Reveal That Aging Exacerbates ARDS Through
Qing Liu1, Cheng Yin1, Long Fan1
1Department of Anesthesiology, Xuanwu Hospital, Capital Medical University, Beijing, People's Republic of China.
Journal of Inflammation Research
|April 23, 2026
Summary
Aging worsens Acute Respiratory Distress Syndrome (ARDS) by amplifying a MAPK14/ADM/MAPK8 signaling pathway, leading to increased inflammation and lung damage. Targeting this pathway offers a potential therapy for older ARDS patients.
Area of Science:
- Immunology
- Molecular Biology
- Gerontology
Background:
- Aging is a significant risk factor that exacerbates Acute Respiratory Distress Syndrome (ARDS) severity.
- The precise molecular mechanisms underlying age-related ARDS exacerbation remain incompletely understood.
Purpose of the Study:
- To elucidate the molecular mechanisms by which aging worsens ARDS.
- To identify and validate a novel signaling axis involving MAPK14, ADM, and MAPK8 in age-related ARDS.
Main Methods:
- Integrated analysis of ARDS gene expression data focusing on aging and immune genes.
- Functional enrichment, machine learning, transcription factor prediction, and immune infiltration analysis.
- Validation in a murine ARDS model using young and aged mice.
Main Results:
- A novel MAPK14/ADM/MAPK8 signaling axis was identified, with MAPK8 downregulated and MAPK14/ADM upregulated in ARDS.
- Aging significantly exacerbated ARDS severity, with more pronounced MAPK14/ADM upregulation and MAPK8 downregulation in aged mice.
- Fostamatinib was identified as a potential therapeutic agent targeting the ARDS-associated expression signature.
Conclusions:
- A novel MAPK14/ADM/MAPK8 signaling axis is a key mechanism in age-related inflammatory dysregulation in ARDS.
- Aging amplifies this pro-inflammatory pathway, worsening lung tissue damage.
- Targeting this axis presents a promising therapeutic strategy for elderly ARDS patients.
Related Concept Videos
01:07MAPK Signaling Cascades
7.3K
Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
7.3K
01:23Chronic Obstructive Pulmonary Disease II: Emphysema
19
Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.PathophysiologyIt most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke.
19
01:30Acute Respiratory Failure-III
1.3K
Hypercapnic respiratory failure, also known as Type 2 or ventilatory respiratory failure, is a severe condition characterized by the body's inability to effectively remove carbon dioxide (CO2) from the bloodstream. It leads to an arterial CO2 pressure (PaCO2) exceeding 45 mmHg and a blood pH above 7.35. This situation indicates that the body's ventilatory demand, or the ventilation needed to maintain normal PaCO2 levels, surpasses its supply or the maximum gas flow achievable without...
1.3K
01:24Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features
28
Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...
28
01:29Acute Respiratory Failure-V
730
The treatment for acute respiratory failure varies based on factors like the underlying cause, overall health, and severity. A collaborative healthcare team is essential for early detection, often through arterial blood gas analysis. Identifying the cause is the primary goal, with treatment strategies adjusted for ventilation/perfusion (V/Q) mismatch, shunting, or diffusion impairment.
Ensure that patients are monitored continuously for their response to therapy, including changes in...
Ensure that patients are monitored continuously for their response to therapy, including changes in...
730
01:20Chronic Obstructive Pulmonary Disease-II: Pathophysiology
4.9K
Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
Chronic Inflammation
4.9K