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Healing II: Complications01:24

Healing II: Complications

Complications during healing arise when tissue repair is altered by local or systemic factors. These changes involve abnormal collagen deposition, altered biomechanics, and reduced vascular supply, impairing restoration of normal structure and function.Loss of FunctionScar tissue differs significantly from the original tissue it replaces. In the skin, fibrosis lacks adnexal structures such as hair follicles, sebaceous glands, and sweat glands. Their absence reduces tactile sensitivity, impairs...

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Related Experiment Video

Updated: Jun 17, 2026

Ex Vivo Corneal Organ Culture Model for Wound Healing Studies
06:46

Ex Vivo Corneal Organ Culture Model for Wound Healing Studies

Published on: February 15, 2019

Pathological Interplay of ROS With Myofibroblasts: An Impediment to Corneal Restitution.

Mohammad Yahya Karimi1, Abasalt Hosseinzadeh Colagar1

  • 1Department of Molecular and Cell Biology, Faculty of Basic Science, University of Mazandaran, Babolsar, Iran, umz.ac.ir.

Oxidative Medicine and Cellular Longevity
|June 16, 2026
PubMed
Summary

Dysregulated reactive oxygen species (ROS) drive myofibroblast persistence, hindering tissue repair. Targeting ROS offers a promising therapeutic strategy for improving corneal recovery after injury.

Keywords:
corneahealingmyofibroblastpathogenesisreactive oxygen species

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Last Updated: Jun 17, 2026

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Full-Field Optical Coherence Microscopy for Histology-Like Analysis of Stromal Features in Corneal Grafts

Published on: October 21, 2022

Area of Science:

  • Cell biology
  • Tissue repair mechanisms
  • Biochemistry

Background:

  • Myofibroblasts are crucial for tissue repair but can cause complications like corneal fibrosis when persistent.
  • Reactive oxygen species (ROS) are signaling molecules involved in myofibroblast function.

Purpose of the Study:

  • To investigate the pathological role of dysregulated ROS in myofibroblast persistence and corneal fibrosis.
  • To explore targeting ROS as a therapeutic strategy for corneal recovery.

Main Methods:

  • Review of cellular events and molecular mechanisms involving ROS and myofibroblasts.
  • Analysis of ROS-mediated modulation of extracellular matrix (ECM) remodeling and immune responses.
  • Examination of ROS impact on myofibroblast survival, apoptosis, and senescence.

Main Results:

  • Dysregulated ROS promote myofibroblast differentiation, ECM remodeling, and immune evasion, leading to self-perpetuating survival cycles.
  • ROS enhance ECM stiffness and resistance to apoptosis, induce senescence, and impair immune clearance of myofibroblasts.
  • ROS alter ECM components like proteoglycans and glycosaminoglycans, favoring myofibroblast persistence.

Conclusions:

  • Dysregulated ROS contribute significantly to myofibroblast persistence and pathological tissue remodeling.
  • Targeting ROS presents a potential therapeutic avenue to mitigate myofibroblast-driven complications and promote corneal healing.