Glucocorticoid and mineralocorticoid receptor expression in critical illness: A narrative review.
Level 5 - mechanism / opinion, no new human data
Narrative review without systematic methodology or primary human data
PubMed 34316445 · doi:10.5492/wjccm.v10.i4.102
What was done
The authors conducted a narrative review of clinical literature exploring the roles and expression of glucocorticoid receptors, mineralocorticoid receptors, and 11β-hydroxysteroid dehydrogenase isozymes (types 1 and 2) in the inflammatory response during critical illness.
What was found
The abstract reports no numerical findings or quantitative metrics. It describes the physiology of hypothalamic-pituitary-adrenal axis activation in critical illness, noting that while circulating cortisol is often elevated, some patients exhibit disproportionately low levels. It describes how receptor dysfunction can lead to tissue glucocorticoid resistance and that intracellular cortisol availability differs from circulating levels due to local interconversion with inert cortisone by 11β-hydroxysteroid dehydrogenases.
Why it matters
This review highlights that systemic cortisol levels do not fully capture tissue-specific corticosteroid signaling, which depends heavily on local receptor expression and enzymatic conversion.
Limits
The paper is a narrative review with no systematic search criteria, meta-analytic pooling, or quality appraisal reported in the abstract. No sample sizes, patient demographics, or quantitative outcome measures are provided.
Cited by
- supports Cortisol binds to intracellular receptors—the glucocorticoid receptor (GR) and mineralocorticoid receptor (MR)—which act as transcription factors that translocate to the nucleus to regulate gene expression.