The DOI matches its Crossref record; 282 of the 282 references it cites were found in a registry or an index.
Inflammatory Process in Type 2 Diabetes: The Role of Cytokines
Abstract
Abstract: Population‐based studies have shown strong relationship between inflammatory markers and metabolic disturbances, obesity, and atherosclerosis, whereas inflammation has been considered as a “common soil” between these clinical entities and type 2 diabetes (T2D). The accumulation of macrophages in adipose tissue (AT), the common origin of macrophages and adipocytes, the prevalent presence of peripheral mononuclear cells, and apoptotic β cells by themselves seem to be the sources of inflammation present in T2D, since they generate the mediators of the inflammatory processes, namely cytokines. The main cytokines involved in the pathogenesis of T2D are interleukin‐1β (IL‐1β), with an action similar to the one present in type 1 diabetes, tumor necrosis factor‐α (TNF‐α), and IL‐6, considered as the main regulators of inflammation, leptin, more recently introduced, and several others, such as monocyte chemoattractant protein‐1, resistin, adiponectin, with either deleterious or beneficial effects in diabetic pathogenesis. The characterization of these molecules targeted diabetes treatment beyond the classical interventions with lifestyle changes and pharmaceutical agents, and toward the determination of specific molecular pathways that lead to low grade chronic inflammatory state mainly due to an immune system's unbalance.
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“Type 2 diabetes, obesity, and cardiovascular disease are related to a state of low-grade systemic inflammation [7, 27–29].”
From Exercise as a Mean to Control Low‐Grade Systemic Inflammation (2008) · cites this paper as [29]
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“Thus, a number of studies indicate that elevated TNF-α is not secondary to the pathological conditions associated with insulin resistance, but that TNF-α plays a direct pathogenic role in glucose metabolism [29, 40].”
From Exercise as a Mean to Control Low‐Grade Systemic Inflammation (2008) · cites this paper as [29]
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Metadata
- Authors
- ALEXANDRAKI, K., PIPERI, C., KALOFOUTIS, C., SINGH, J., ALAVERAS, A., & KALOFOUTIS, A.
- Affiliations
- National and Kapodistrian University of Athens (GR)
- University of Lancashire (GB)
- Corresponding author
- PIPERI, CHRISTINA
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2006-11
- Volume
- 1084
- Issue
- 1
- Pages
- 89-117
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- OpenAlex
- W1491280754
- Semantic Scholar
- 160271b5b2f5d455bde3b3b6558683292a30fa1c
- Cited by
- 309
- References
- 281
- Citations by year
- 2026: 7 · 2025: 9 · 2024: 21 · 2023: 13 · 2022: 11 · 2021: 16 · 2020: 12 · 2019: 11 · 2018: 19 · 2017: 15 · 2016: 17 · 2015: 14 · 2014: 22 · 2013: 20 · 2012: 14
- FWCI
- 2.18
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of the New York Academy of Sciences (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- type 2 diabetes, inflammation, adipose tissue macrophages, cytokines, IL-1β, TNF-α, interleukin-6, leptin, adiponectin, resistin, MCP-1, beta-cell apoptosis, obesity, atherosclerosis, low-grade inflammation, immune dysregulation
- MeSH terms
- Animals, Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 2, Humans, Inflammation, Cytokines
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