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Related Concept Videos

Inflammation01:38

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Overview
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The thoracic section of the aorta begins at the T5 vertebra and extends to the T12 level at the diaphragm, initially progressing through the mediastinum to the left of the spinal column. Throughout its course in the thoracic segment, the thoracic aorta emits various offshoots known collectively as visceral and parietal branches. The branches that predominantly supply blood to visceral organs are termed visceral branches and include bronchial, pericardial, esophageal, and mediastinal arteries,...
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Aneurysm I: Introduction01:30

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An aortic aneurysm is a localized outpouching or dilation at a weak point in the artery wall. It may involve different parts of the aorta, such as the abdominal aorta, aortic arch, or thoracic aorta.Etiological factorsSeveral disorders are associated with aortic aneurysms.Congenital causes, such as primary connective tissue disorders like Marfan syndrome, impact the integrity and strength of connective tissues, notably affecting the aorta. Marfan syndrome is a genetic disorder that specifically...
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The thoracic or rib cage forms the body's thorax (chest) portion. Its primary function in the body is to protect vital organs in the thoracic cavity, such as the heart and the lungs. It consists of 12 pairs of ribs with their costal cartilages and the sternum. The ribs are anchored posteriorly to the 12 thoracic vertebrae (T1-T12).
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Ribs are curved, flattened bones forming the thoracic cavity wall with the thoracic muscles. There are 12 pairs of thoracic ribs. The posterior ends of all the ribs articulate with the T1–T12 thoracic vertebrae. In contrast,the anterior ends of most ribs attach to the sternum via their costal cartilages.
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Breathing, otherwise known as pulmonary ventilation, is the process of air movement into and out of the lungs. The main mechanisms propelling pulmonary ventilation are atmospheric pressure (Patm), intra-pulmonary (Ppul ) or intra-alveolar pressure (Palv) within the alveoli, and intrapleural pressure (Pip) within the pleural cavity.
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Related Experiment Video

Updated: Jan 29, 2026

Murine Surgical Model of Topical Elastase Induced Descending Thoracic Aortic Aneurysm
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Inflammation in thoracic aortic aneurysms.

N E H Dinesh1, D P Reinhardt2,3

  • 1Faculty of Medicine, Department of Anatomy and Cell Biology and Faculty of Dentistry, McGill University, Montreal, Canada.

Herz
|February 13, 2019
PubMed
Summary

Genetic mutations compromise the aortic wall in Marfan syndrome, leading to defective mechanosensing and inflammation. Targeting inflammation and specific signaling pathways may prevent thoracic aortic aneurysm progression.

Keywords:
Angiotensin IIAnti-inflammatory agentsAortic diseasesExtracellular matrixTransforming growth factor-beta

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Area of Science:

  • Cardiovascular Biology
  • Genetics
  • Pathology

Background:

  • Marfan syndrome (MFS) and related disorders involve mutations in extracellular matrix and smooth muscle cell proteins, compromising the aortic wall.
  • These genetic defects lead to abnormal aortic tissue mechanosensing under hemodynamic stress, involving transforming growth factor-beta (TGF-β) and angiotensin-II (Ang-II) signaling pathways.

Purpose of the Study:

  • To investigate the role of inflammation and signaling pathways in the pathogenesis of thoracic aortic aneurysms in MFS.
  • To explore potential therapeutic targets for mitigating disease progression.

Main Methods:

  • Analysis of genetic alterations, mechanosensing defects, and downstream signaling pathways in MFS-related aortic disease.
  • Utilizing mouse models to assess the impact of aortic inflammation and therapeutic interventions.
  • Evaluating the effects of targeting TGF-β, Ang-II, and inflammatory pathways.

Main Results:

  • Aberrant mechanosensing is linked to TGF-β hyperactivity, Ang-II signaling, and other cellular perturbations, resulting in proteolytic activity, inflammation, and smooth muscle cell apoptosis.
  • Aortic inflammation is a key factor in aneurysm development, as shown in mouse models.
  • Inhibition of inflammatory cytokines and specific signaling pathways (ERK1/2, mTOR, PI3/Akt, P38/MAPK, Rho kinase) attenuated disease pathogenesis.

Conclusions:

  • Treating inflammation associated with thoracic aortic aneurysms in MFS and related disorders may be beneficial.
  • Targeting specific downstream signaling pathways offers a promising therapeutic strategy for limiting disease progression.