From immune activation to disease progression : Unraveling the complex role of Serum Amyloid A proteins
(2025) In Cytokine & Growth Factor Reviews- Abstract
Serum Amyloid A (SAA) proteins are critical mediators of immune activation and metabolic regulation, bridging the acute-phase response with long-term disease dynamics. Once considered mere biomarkers of inflammation, emerging research has revealed their central role in orchestrating immune responses, lipid metabolism, and tissue remodeling. SAA proteins display context-dependent functions: they promote immune defense and tissue regeneration in some conditions, while exacerbating chronic inflammation and disease progression in others. Recent studies highlight the intricate interplay between SAA isoforms, pattern recognition receptors, and metabolic pathways, with implications for autoimmune diseases, metabolic disorders, and inflammatory... (More)
Serum Amyloid A (SAA) proteins are critical mediators of immune activation and metabolic regulation, bridging the acute-phase response with long-term disease dynamics. Once considered mere biomarkers of inflammation, emerging research has revealed their central role in orchestrating immune responses, lipid metabolism, and tissue remodeling. SAA proteins display context-dependent functions: they promote immune defense and tissue regeneration in some conditions, while exacerbating chronic inflammation and disease progression in others. Recent studies highlight the intricate interplay between SAA isoforms, pattern recognition receptors, and metabolic pathways, with implications for autoimmune diseases, metabolic disorders, and inflammatory pathologies. Despite their well-documented role in acute inflammation, the therapeutic potential of SAA proteins remains underexplored. Ongoing research aims to dissect their multifaceted functions and isoform-specific effects, paving the way for novel diagnostic and therapeutic strategies in immune-mediated diseases.
(Less)
- author
- Papareddy, Praveen
LU
and Herwald, Heiko LU
- organization
- publishing date
- 2025-04-03
- type
- Contribution to journal
- publication status
- epub
- subject
- in
- Cytokine & Growth Factor Reviews
- publisher
- Elsevier
- external identifiers
-
- scopus:105002671724
- pmid:40240198
- ISSN
- 1359-6101
- DOI
- 10.1016/j.cytogfr.2025.03.003
- language
- English
- LU publication?
- yes
- additional info
- Copyright © 2025 The Authors. Published by Elsevier Ltd.. All rights reserved.
- id
- d0d33e90-f561-4480-9ce2-905bce65bc21
- date added to LUP
- 2025-05-01 14:40:24
- date last changed
- 2025-05-06 02:58:20
@article{d0d33e90-f561-4480-9ce2-905bce65bc21, abstract = {{<p>Serum Amyloid A (SAA) proteins are critical mediators of immune activation and metabolic regulation, bridging the acute-phase response with long-term disease dynamics. Once considered mere biomarkers of inflammation, emerging research has revealed their central role in orchestrating immune responses, lipid metabolism, and tissue remodeling. SAA proteins display context-dependent functions: they promote immune defense and tissue regeneration in some conditions, while exacerbating chronic inflammation and disease progression in others. Recent studies highlight the intricate interplay between SAA isoforms, pattern recognition receptors, and metabolic pathways, with implications for autoimmune diseases, metabolic disorders, and inflammatory pathologies. Despite their well-documented role in acute inflammation, the therapeutic potential of SAA proteins remains underexplored. Ongoing research aims to dissect their multifaceted functions and isoform-specific effects, paving the way for novel diagnostic and therapeutic strategies in immune-mediated diseases.</p>}}, author = {{Papareddy, Praveen and Herwald, Heiko}}, issn = {{1359-6101}}, language = {{eng}}, month = {{04}}, publisher = {{Elsevier}}, series = {{Cytokine & Growth Factor Reviews}}, title = {{From immune activation to disease progression : Unraveling the complex role of Serum Amyloid A proteins}}, url = {{http://dx.doi.org/10.1016/j.cytogfr.2025.03.003}}, doi = {{10.1016/j.cytogfr.2025.03.003}}, year = {{2025}}, }