Functions of arginase isoforms in macrophage inflammatory responses: impact on cardiovascular diseases and metabolic disorders
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Macrophages play a paramount role in immunity and inflammation-associated diseases, including infections, cardiovascular diseases, obesity-associated metabolic imbalances, and cancer. Compelling evidence from studies of recent years demonstrates that macrophages are heterogeneous and undergo heterogeneous phenotypic changes in response to microenvironmental stimuli. The M1 killer type response and the M2 repair type response are best known, and are two extreme examples. Among other markers, inducible nitric oxide synthase and type-I arginase (Arg-I), the enzymes that are involved in l-arginine/nitric oxide (NO) metabolism, are associated with the M1 and M2 phenotype, respectively, and therefore widely used as the markers for characterization of the two macrophage phenotypes. There is also a type-II arginase (Arg-II), which is expressed in macrophages and prevalently viewed as having the same function as Arg-I in the cells. In contrast to Arg-I, little information on the role of Arg-II in macrophage inflammatory responses is available. Emerging evidence, however, suggests that differential roles of Arg-I and Arg-II in regulating macrophage functions. In this article, we will review recent developments on the functional roles of the two arginase isoforms in regulation of macrophage inflammatory responses by focusing on their impact on the pathogenesis of cardiovascular diseases and metabolic disorders.
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ARG1 in myeloid cells mainly functions as an enzyme to hydrolyze arginine to produce ornithine as part of the urea cycle, which promotes tissue repair through generation of polyamines and collagens, and reduces nitric oxide production from inducible nitric oxide synthase through decreasing intracellular arginine availability.
“ARG1 in myeloid cells mainly functions as an enzyme to hydrolyze arginine to produce ornithine as part of the urea cycle, which both promotes tissue repair through generation of polyamines and collagens, and also reduces nitric oxide production from inducible nitric oxide synthase through decreasing intracellular arginine availability (76–78).”
From <i>Trem2</i> promotes anti-inflammatory responses in microglia and is suppressed under pro-inflammatory conditions (2020) · cites this paper as [76]
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- Authors
- Yang, Z., & Ming, X.-F.
- Affiliations
- University of Fribourg (CH)
- Corresponding author
- Yang, Zhihong
- Ming, Xiu-Fen
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2014-10-27
- Volume
- 5
- Pages
- 533-533
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC4209887
- OpenAlex
- W2018261122
- Cited by
- 290
- References
- 107
- Citations by year
- 2026: 20 · 2025: 31 · 2024: 32 · 2023: 39 · 2022: 30 · 2021: 29 · 2020: 40 · 2019: 23 · 2018: 15 · 2017: 16 · 2016: 5 · 2015: 10
- FWCI
- 1.01
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Immunology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Science Foundation (120435, 310030)
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (310000-120435/1, 141070, 120435, 310000, 310030)
- Schweizerische Herzstiftung
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Keywords
- macrophage polarization, M1/M2 macrophage phenotype, inducible nitric oxide synthase, macrophage inflammation, cardiovascular disease, metabolic disorders, obesity
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