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Rheumatic Heart Disease I: Introduction

Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
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Chronic Inflammation
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Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
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Related Experiment Video

Updated: May 24, 2026

Refined Murine Model of Idiopathic Pulmonary Fibrosis
07:51

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Published on: June 17, 2025

Inflammation-driven mitochondrial dysfunction and ROS accumulation orchestrate pulmonary fibrotic remodeling in

Zhaoqian Zhong1, Kan Wu2, Junhao Wang2

  • 1State Key Laboratory of Metabolic Dysregulation & Prevention and Treatment of Esophageal Cancer, Henan Key Laboratory of Critical Care Medicine, Henan International Joint Laboratory of Infection and Immunology, Department of Emergency Medicine, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, 450001, China; Institute of Infection and Immunity, Henan Academy of Innovations in Medical Science, Zhengzhou, 451163, China; Department of Respiratory and Critical Care Medicine, The Tenth Affiliated Hospital, Southern Medical University, Dongguan, 523058, China; Guangdong Provincial Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.

Redox Biology
|May 22, 2026
PubMed
Summary

Early pulmonary fibrosis in sepsis is driven by sustained inflammation and mitochondrial dysfunction. Key genes regulating reactive oxygen species (ROS) and specific Col13a1+ fibroblasts initiate lung scarring.

Keywords:
Mitochondrial disfunctionMulti-omics analysisPulmonary fibrosisReactive oxygen speciesSepsis

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Bronchoalveolar Lavage Exosomes in Lipopolysaccharide-induced Septic Lung Injury
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Bronchoalveolar Lavage Exosomes in Lipopolysaccharide-induced Septic Lung Injury

Published on: May 21, 2018

Area of Science:

  • Pulmonary Medicine
  • Immunology
  • Mitochondrial Biology

Background:

  • Pulmonary fibrosis is a severe, irreversible lung disease with unclear early mechanisms.
  • Sepsis-induced inflammation can lead to significant lung function decline and mortality.

Purpose of the Study:

  • To elucidate the early pathogenesis of inflammation-induced pulmonary fibrosis.
  • To identify key molecular drivers and cellular players in sepsis-related lung fibrosis.

Main Methods:

  • Integration of multi-omics data and animal models.
  • Mitochondria-related gene analysis and temporal data analysis.
  • In vitro assays, bulk and single-cell transcriptomic analyses.

Main Results:

  • Lungs show heightened immune response and mitochondrial dysfunction during inflammation, initiating fibrotic signaling.
  • Six key genes in reactive oxygen species (ROS) metabolism were identified and linked to sepsis outcomes.
  • Sustained TNF-α/IL-1β signaling drives ROS accumulation, causing cellular damage and fibroblast reprogramming.
  • Col13a1+ fibroblasts were identified as a critical subpopulation driving fibrotic remodeling.

Conclusions:

  • Sustained TNF-α/IL-1β signaling and ROS accumulation initiate pulmonary fibrosis in sepsis.
  • Col13a1+ fibroblasts are a major profibrotic cell type in this process.
  • Targeting TNF-α/IL-1β, ROS, and Col13a1+ fibroblasts offers potential therapeutic strategies for sepsis-induced pulmonary fibrosis.