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Hypothalamic-Pituitary Axis01:37

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The response to stress—be it physical or psychological, acute or chronic—involves activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis. The HPA axis is part of the neuroendocrine system because it involves both neuronal and hormonal communication. Its function is to regulate homeostatic systems—metabolic, cardiovascular, and immune—providing the necessary means to respond to a stressor.
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Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features...
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Hyperthyroidism II: Pathophysiology01:27

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Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH...
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Hypothyroidism II: Pathophysiology01:23

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Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
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Cushing Syndrome I: Introduction01:26

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Cushing syndrome refers to the collection of clinical manifestations that arise when tissues are exposed to excessive amounts of cortisol or cortisol-like medications over an extended period. Cortisol, a glucocorticoid produced by the adrenal cortex, regulates metabolism, immune responses, and the body’s adaptation to stress. When its concentration remains chronically elevated, these physiological pathways become dysregulated, resulting in the characteristic features of the...
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Hormonal Regulation of the Menstrual Cycle01:22

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The ovarian cycle regulates endometrial changes throughout a single menstrual cycle via the coordinated action of gonadotrophin-releasing hormone (GnRH) and gonadotrophins.
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Erythroid-hormonal axis in long COVID.

Shokrollah Elahi1

  • 1Division of Foundational Sciences, Mike Petryk School of Dentistry, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, Alberta T6G 2E1, Canada; Li Ka Shing Institute of Virology, University of Alberta, Edmonton, Alberta T6G 2E1, Canada; Women and Children Health Research Institute, University of Alberta, Edmonton, Alberta T6G 2E1, Canada; Cancer Research Institute of Northern Alberta, University of Alberta, Edmonton, Alberta T6G 2E1, Canada; Glycomics Institute of Alberta, University of Alberta, Edmonton, Alberta T6G 2E1, Canada; Alberta Transplant Institute, University of Alberta, Edmonton, Alberta T6G 2E1, Canada.

Trends in Molecular Medicine
|May 5, 2026
PubMed
Summary

Long COVID might stem from impaired physiological recovery, not persistent infection. Key mechanisms involve inflammation disrupting red blood cell production and hormone balance, offering new therapeutic targets.

Keywords:
CD71(+) erythroid cellsME/CFSsex hormones

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Area of Science:

  • Immunology
  • Endocrinology
  • Hematology

Background:

  • Long COVID symptoms may arise from dysregulated physiological recovery processes.
  • Emerging evidence suggests inflammation plays a critical role in persistent Long COVID symptoms.

Purpose of the Study:

  • To explore the role of erythroid-endocrine pathways in Long COVID.
  • To identify potential therapeutic targets for Long COVID recovery.

Main Methods:

  • Review of emerging evidence on Long COVID pathophysiology.
  • Analysis of the link between immune dysregulation, metabolic stress, and hormonal imbalance.

Main Results:

  • Inflammation-driven disruption of erythropoiesis (red blood cell production) is implicated.
  • Hormonal imbalance is identified as a central mechanism in Long COVID.

Conclusions:

  • Erythroid-endocrine pathways are crucial for Long COVID recovery.
  • Targeting these pathways may offer novel therapeutic strategies for Long COVID.