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Related Concept Videos

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...

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Related Experiment Video

Updated: Jun 6, 2026

Isolation of Human Lymphatic Endothelial Cells by Multi-parameter Fluorescence-activated Cell Sorting
07:36

Isolation of Human Lymphatic Endothelial Cells by Multi-parameter Fluorescence-activated Cell Sorting

Published on: May 1, 2015

Pulmonary lymphangioleiomyomatosis.

Xuchen Zhang1, William D Travis

  • 1Department of Pathology, State University of New York, Downstate Medical Center, Brooklyn, 11203, USA. xuchen.zhang@downstate.edu

Archives of Pathology & Laboratory Medicine
|December 7, 2010
PubMed
Summary

Lymphangioleiomyomatosis (LAM) is a rare lung disease in women caused by abnormal cell growth. Mutations in TSC1/TSC2 genes are linked to LAM, offering potential new therapeutic targets.

Area of Science:

  • Pulmonary Medicine
  • Oncology
  • Genetics

Background:

  • Lymphangioleiomyomatosis (LAM) is a rare lung disease affecting women of childbearing age.
  • Characterized by proliferation of smooth muscle-like cells causing lung destruction and pulmonary dysfunction.
  • LAM cells express both smooth muscle and melanocytic markers.

Purpose of the Study:

  • To summarize the key features and pathogenesis of Lymphangioleiomyomatosis.
  • To highlight the association between LAM and tuberous sclerosis complex (TSC) genes.
  • To identify potential therapeutic targets for LAM.

Main Methods:

  • Review of existing literature on Lymphangioleiomyomatosis.
  • Analysis of cellular markers and genetic mutations associated with LAM.

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Isolation of Human Lymphatic Endothelial Cells by Multi-parameter Fluorescence-activated Cell Sorting
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Chronic Thromboembolic Pulmonary Hypertension and Assessment of Right Ventricular Function in the Piglet

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  • Investigation of TSC1/TSC2 signaling pathways in disease pathogenesis.

    • Main Results:

    • LAM involves abnormal smooth muscle-like cell proliferation leading to cystic lung destruction.
    • Common clinical features include dyspnea and pneumothorax.
    • Mutations in TSC1 or TSC2 tumor suppressor genes are strongly linked to LAM.

    Conclusions:

    • The TSC1/TSC2 pathway is implicated in LAM pathogenesis.
    • Understanding these pathways may lead to novel therapeutic strategies for LAM.
    • Targeting TSC1/TSC2 dysfunction offers promise for treating LAM and related disorders.