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Related Concept Videos

Atelectasis II: Pathophysiology01:10

Atelectasis II: Pathophysiology

Atelectasis develops when alveoli lose their air and collapse inward. Because lung tissue is naturally elastic, these air sacs shrink rather than remaining open. Collapsed alveoli are no longer ventilated, reducing their role in gas exchange. Blood flow may continue in these regions, creating a ventilation–perfusion mismatch. Clinical findings include decreased breath sounds, dullness to percussion, reduced chest expansion, and decreased tactile fremitus as sound transmission through collapsed...
Pneumothorax II: Pathophysiology01:08

Pneumothorax II: Pathophysiology

Pneumothorax means the presence of air in the pleural space — the thin potential gap between the visceral and parietal pleura. This condition disrupts the normal pressure balance that keeps the lungs inflated, leading to partial or complete collapse of the affected lung.Normal physiologyUnder normal conditions, the pleural space maintains a slightly negative intrapleural pressure, which keeps the lungs expanded against the chest wall. This negative pressure creates a delicate balance between...
Pulmonary Hypertension: Classification and Pathogenesis01:30

Pulmonary Hypertension: Classification and Pathogenesis

Pulmonary hypertension (PH) is a severe health condition in which the mean pulmonary arterial pressure increases to 25 mmHg or more, even when the body is at rest. This high pressure in the blood vessels that transport blood from the heart to the lungs can cause various symptoms, including shortness of breath, can lead to right heart failure, and significantly affect the overall quality of life.
There are various classifications for PH, each relating to different underlying causes and also...
Pulmonary Edema II: Pathophysiology01:18

Pulmonary Edema II: Pathophysiology

Pulmonary edema is the accumulation of fluid in the interstitial and alveolar spaces of the lungs, impairing gas exchange and oxygen delivery. It may be cardiogenic or noncardiogenic, but both reduce oxygenation and lung compliance.Cardiogenic Pulmonary EdemaCardiogenic edema results from increased hydrostatic pressure in pulmonary capillaries, usually due to left ventricular dysfunction from myocardial infarction, heart failure, or valvular disease. Ineffective cardiac pumping causes blood to...
Pneumonia II: Pathophysiology01:29

Pneumonia II: Pathophysiology

The pathophysiology of pneumonia involves the following steps:

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Related Experiment Video

Updated: Jun 9, 2026

Open Tracheostomy Gastric Acid Aspiration Murine Model of Acute Lung Injury Results in Maximal Acute Nonlethal Lung Injury
09:16

Open Tracheostomy Gastric Acid Aspiration Murine Model of Acute Lung Injury Results in Maximal Acute Nonlethal Lung Injury

Published on: February 26, 2017

Acute Lung Injury: From Molecular Circuits to System-Level Therapeutics.

Yaoli Hou1,2, Sheng He3, Lili He2,4

  • 1Department of Medical Administration The Second Affiliated Hospital University of South China Hengyang Hunan China.

Medcomm
|June 8, 2026
PubMed
Summary

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are complex network disorders. New research redefines ALI/ARDS by integrating immunity, metabolism, and cell death networks for targeted therapies.

Keywords:
PANoptosisacute lung injury (ALI)endotypesimmunometabolismnetwork medicine

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Area of Science:

  • Pulmonary Medicine
  • Immunology
  • Systems Biology

Background:

  • Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are critical conditions with high mortality.
  • Current therapeutic failures are linked to reductionist approaches targeting isolated pathways.

Purpose of the Study:

  • To synthesize recent breakthroughs in understanding ALI/ARDS as integrated pathological networks.
  • To redefine ALI/ARDS by analyzing interconnected circuits in immunity, metabolism, and cell death.
  • To explore the role of multiorgan communication in pulmonary inflammation.

Main Methods:

  • Systematic analysis of interconnected biological networks (cGAS-STING, immunometabolism, programmed cell death).
  • Integration of single-cell technologies, multiomics profiling, and computational modeling.
  • Deconstruction of ARDS heterogeneity into distinct endotypes.

Main Results:

  • ALI/ARDS are characterized by dysregulated networks involving immunity, metabolism, and cell death (e.g., PANoptosis).
  • The brain and gut actively influence pulmonary inflammation in ALI/ARDS.
  • ARDS heterogeneity is deconstructed into clinically actionable endotypes (C1, C2) with differential treatment responses.

Conclusions:

  • A network-based understanding of ALI/ARDS necessitates a shift toward mechanism-based, personalized interventions.
  • Future therapies may involve poly-pharmacology, precision immunotherapies, and advanced nanomaterial platforms.
  • This holistic approach aims to move beyond supportive care towards genuine disease modification for ALI/ARDS.