Hypercapnia Regulates Gene Expression and Tissue Function

Masahiko Shigemura, Lynn C. Welch, Jacob I. Sznajder*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

Abstract

Carbon dioxide (CO2) is produced in eukaryotic cells primarily during aerobic respiration, resulting in higher CO2 levels in mammalian tissues than those in the atmosphere. CO2 like other gaseous molecules such as oxygen and nitric oxide, is sensed by cells and contributes to cellular and organismal physiology. In humans, elevation of CO2 levels in tissues and the bloodstream (hypercapnia) occurs during impaired alveolar gas exchange in patients with severe acute and chronic lung diseases. Advances in understanding of the biology of high CO2 effects reveal that the changes in CO2 levels are sensed in cells resulting in specific tissue responses. There is accumulating evidence on the transcriptional response to elevated CO2 levels that alters gene expression and activates signaling pathways with consequences for cellular and tissue functions. The nature of hypercapnia-responsive transcriptional regulation is an emerging area of research, as the responses to hypercapnia in different cell types, tissues, and species are not fully understood. Here, we review the current understanding of hypercapnia effects on gene transcription and consequent cellular and tissue functions.

Original languageEnglish (US)
Article number598122
JournalFrontiers in Physiology
Volume11
DOIs
StatePublished - Nov 20 2020

Keywords

  • carbon dioxide
  • cellular and tissue function
  • hypercapnia
  • innate immune system
  • lung
  • skeletal muscles
  • transcriptional regulation

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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