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Cellular crosstalk in cardioprotection: Where and when do reactive oxygen species play a role?

Tania Martins-Marques1, Antonio Rodriguez-Sinovas2, Henrique Girao1

  • 1Univ Coimbra, Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, Coimbra, Portugal; Univ Coimbra, Center for Innovative Biomedicine and Biotechnology (CIBB), Coimbra, Portugal; Clinical Academic Centre of Coimbra (CACC), Coimbra, Portugal.

Free Radical Biology & Medicine
|April 23, 2021
PubMed

Insights

Reactive oxygen species (ROS) disrupt cardiac cell communication after heart attacks. This review explores how ROS impact intercellular signaling, gap junctions, and extracellular vesicles in myocardial reperfusion injury.

Area of Science:

  • Cardiovascular Biology
  • Cellular Signaling

Background:

  • Intercellular communication is crucial for cardiac homeostasis.
  • Acute myocardial infarction is a leading cause of mortality worldwide.
  • Reperfusion therapy, while vital, can cause myocardial reperfusion injury due to reactive oxygen species (ROS).

Purpose of the Study:

  • To discuss the impact of ROS on intercellular and intracellular communication in the heart.
  • To explore the role of gap junctions, tunneling nanotubes, and extracellular vesicles in propagating oxidative damage.
  • To highlight the significance of these processes in cardiac diseases, especially ischemia/reperfusion injury.

Main Methods:

  • Review of existing literature on ROS, cardiac cell communication, and myocardial reperfusion injury.
  • Analysis of the roles of gap junctions, tunneling nanotubes, and extracellular vesicles in oxidative stress propagation.
  • Synthesis of current understanding of ROS signaling in cardiac cell-cell crosstalk.

Main Results:

  • ROS significantly impact various forms of cell-cell communication within the heart.
  • Gap junctions, tunneling nanotubes, and extracellular vesicles are implicated in the spread of oxidative damage.
  • ROS signaling pathways are intricately linked to cell differentiation and communication.

Conclusions:

  • Understanding ROS-mediated intercellular communication is vital for managing cardiac diseases.
  • Targeting these communication pathways may offer novel therapeutic strategies for myocardial reperfusion injury.
  • Further research into the specific roles of gap junctions, tunneling nanotubes, and EVs in ROS propagation is warranted.

Keywords:
Cardiovascular diseasesConnexinExtracellular vesiclesGap junctionsHeartIntercellular communicationIntracellular communicationOxidative stress

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