From Fat to Flame: Targeting Adipose Tissue in Chronic Inflammation and Exploring Therapeutic Strategies

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: 29 May 2026 | Viewed by 1163

Special Issue Editors


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Guest Editor
Department of Biomedical Sciences for Health, University of Milan, Milan, Italy
Interests: breast cancer; inflammation; physical exercise; cardiotoxicity; circulating biomarkers
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Biomedical Sciences for Health, University of Milan, Milan, Italy
Interests: obesity; metabolic disorders; biomarkers of cardiovascular diseases; advanced glycation end products
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Cardiovascular and Metabolic Diseases, IRCCS Multimedica, Via Fantoli 16/15, 20135 Milan, Italy
Interests: glycemic variability; redox systems; diabetes; insulin resistance; prediabetes; microRNA; extracellular vesicles; obesity; innate immune response; cutaneous and visceral adipose tissues; inflammation; signaling pathways
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue focuses on the complex interplay between obesity-induced inflammation and its role in the development of various metabolic disorders. Obesity, particularly visceral obesity, is characterized by low-grade chronic inflammation that contributes significantly to the onset of conditions such as atherosclerosis, metabolic syndrome, insulin resistance, type 2 diabetes mellitus (T2DM), and non-alcoholic fatty liver disease. The expansion of visceral adipose tissue (VAT) through adipocyte hypertrophy triggers inflammatory responses that have systemic effects. This Special Issue aims to delve into the molecular pathways and therapeutic opportunities within this context by providing a thorough update of recent biological observations including, but not limited to, the following areas:

  1. Inflammatory Mechanisms in Obesity: An exploration of how VAT expansion leads to chronic inflammation and the systemic effects of cytokine and chemokine release.
  2. The Role of Inflammasomes: An investigation into the activation of inflammasomes, particularly NLR family proteins, and their contribution to obesity-related inflammation and metabolic dysfunction.
  3. The Role of the Immune System: An investigation into the alteration in the activation and dysfunction of infiltrating immune cells.
  4. Clinical Implications and Outcomes: An examination of clinical studies highlighting the impact of DPP-4 inhibitors, GLP-1 analogs, and SGLT2 inhibitors on inflammation markers, endothelial function, and arterial stiffness in patients.
  5. Biomarkers: Identification of markers characterizing and/or predicting obesity-induced inflammation and cardiometabolic diseases, including epigenetic changes and miRNA.
  6. The Impact of Lifestyle Changes on VAT features, obesity-induced inflammation, and associated co-morbidities.
  7. Microbiota and Obesity: An investigation into how gut microbiota affects VAT function and adipose tissue inflammation.

Dr. Francesca Bianchi
Prof. Dr. Elena Dozio
Dr. Lucia La Sala
Guest Editors

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Keywords

  • obesity
  • inflammasomes
  • immune system
  • microbiota

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Published Papers (1 paper)

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Research

18 pages, 3043 KB  
Article
Myeloid GHSR Deficiency Protects Against Thermogenic Impairment in Aging Through Immune Remodeling of Brown Adipose Tissue
by Hye Won Han, Da Mi Kim, Reza Baratiboldaji, Hongying Wang, Zeyu Liu, Zheng Shen, Deepak K. Jha, Tadesse Teferra, Endang M. Septiningsih, Bhimanagouda Patil and Yuxiang Sun
Cells 2026, 15(4), 321; https://doi.org/10.3390/cells15040321 - 9 Feb 2026
Viewed by 731
Abstract
Thermoregulatory dysfunction is a major pathophysiological consequence of aging, affecting many elderly individuals. Growth hormone secretagogue receptor (GHSR) regulates energy homeostasis and immune function. We previously showed that global GHSR deletion improves thermogenic adaptation of brown adipose tissue (BAT) in aging, but the [...] Read more.
Thermoregulatory dysfunction is a major pathophysiological consequence of aging, affecting many elderly individuals. Growth hormone secretagogue receptor (GHSR) regulates energy homeostasis and immune function. We previously showed that global GHSR deletion improves thermogenic adaptation of brown adipose tissue (BAT) in aging, but the responsible cell type remained unclear. GHSR is expressed in macrophages, and its expression in macrophages increases with aging. Here, we studied myeloid-specific Ghsr-deleted male mice (LysM-Cre; Ghsrf/f denoted as “KO”) to assess their metabolic and immune responses to cold stress at young and old ages. Old mice showed impaired thermogenesis, marked by reduced core body temperature under 4 °C cold exposure, a blunted cold-induced increase in glucose levels, reduced BAT mass, and increased infiltration of pro-inflammatory CD38+ macrophages in BAT. In contrast, KO mice exhibited enhanced cold tolerance in both young and old mice. Notably, aged KO mice showed preserved BAT mass and a pronounced shift in resident macrophages toward an anti-inflammatory state. Consistently, aged KO mice showed reduced pro-inflammatory markers (Ccl2, Nos2) and increased expression of the thermogenic gene Ppargc1a and UCP1 protein under cold exposure. Together, these findings demonstrate that macrophage GHSR drives age-associated pro-inflammatory remodeling of BAT, and that its deletion promotes an immune environment favorable for thermogenic activation. Thus, targeting macrophage GHSR may offer a new therapeutic strategy to restore thermogenesis and enhance thermal resilience in aging. Full article
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