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EDITORIAL article

Front. Endocrinol.
Sec. Molecular and Structural Endocrinology
Volume 15 - 2024 | doi: 10.3389/fendo.2024.1519318
This article is part of the Research Topic Pulmonary Fibrosis and Endocrine Factors View all 8 articles

Editorial: Pulmonary Fibrosis and Endocrine Factors

Provisionally accepted
  • 1 Hebei Normal University, Shijiazhuang, China
  • 2 Loyola University Chicago, Chicago, Illinois, United States
  • 3 Yunnan University, Kunming, Yunnan Province, China

The final, formatted version of the article will be published soon.

    Pulmonary fibrosis (PF) is a complex and highly heterogeneous disease characterized by the accumulation of stiffened extracellular matrix in lung tissue, the replacement of normal lung tissue with fibrotic tissue, and the progressive loss of lung function. PF is induced by genetic, environmental, and inflammatory factors and is associated with metabolic disorders. Extracellular bioactive mediators, such as endocrine factors and metabolites, play critical roles in the progression of PF. For instance, iron promotes PF by activating fibroblasts (1). Animal models have also demonstrated that thyroid hormone, brain-derived neurotrophic factor, and atrial natriuretic peptide regulate PF (2)(3)(4). Focusing treatment on dysregulated endocrine factors rather than inhibiting downstream fibrosis markers may be more effective. In addition, supplementing endogenous cytokines or metabolites theoretically results in fewer side effects than exogenous drugs. This research topic, "Pulmonary Fibrosis and Endocrine Factors", aims to define the endogenous factors associated with pulmonary fibrosis in order to facilitate the discovery of novel and effective therapeutic strategies with fewer side effects. This collection addresses the roles of lipid metabolism, glucose metabolism, complement pathway, and serum biomarkers in PF or cystic fibrosis (CF). It also investigates the association of vitamin D metabolism-related single nucleotide polymorphisms with the risk of chronic obstructive pulmonary disease (COPD).

    Keywords: Pulmonary Fibrosis, Apolipoprotein B, Glycolysis, diabetes, complement, Vitamin D

    Received: 29 Oct 2024; Accepted: 31 Oct 2024.

    Copyright: © 2024 Cao, Ji and Sun. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Pengxiu Cao, Hebei Normal University, Shijiazhuang, China
    Hong-Long (James) Ji, Loyola University Chicago, Chicago, 60660, Illinois, United States
    Jianwei Sun, Yunnan University, Kunming, 650500, Yunnan Province, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.