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Updated: Jan 3, 2026

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Foam Cells: One Size Doesn't Fit All.

Valentina Guerrini1, Maria Laura Gennaro1

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Foam cells, linked to chronic inflammation and diseases like tuberculosis, form when macrophages accumulate excess lipids, impairing immune function. Understanding disease-specific foam cell mechanisms is crucial for developing new therapies.

Keywords:
atherosclerosischronic inflammationfoam cellslipid dropletsmacrophagetuberculosis

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Area of Science:

  • Immunology
  • Cell Biology
  • Pathology

Background:

  • Foam cells are characteristic of chronic inflammatory conditions, including infectious diseases, metabolic disorders, and cancers.
  • Their formation involves macrophages exceeding lipid homeostasis, leading to impaired immune functions.
  • Existing knowledge on foam cell formation primarily stems from atherosclerosis research.

Purpose of the Study:

  • To review and compare foam cell formation and function across different disease contexts.
  • To highlight the divergence in biogenesis mechanisms between tuberculosis and atherosclerosis.
  • To underscore the need for disease-specific research for therapeutic targeting.

Main Methods:

  • Literature review of studies on foam cell formation and function.
  • Comparative analysis of foam cell biogenesis in various diseases, focusing on tuberculosis and atherosclerosis.
  • Synthesis of current understanding and identification of knowledge gaps.

Main Results:

  • Foam cell formation and function are context-dependent and vary significantly between diseases.
  • Mechanisms of foam cell biogenesis in tuberculosis differ from those in atherosclerosis.
  • Impaired macrophage immune functions accompany foam cell accumulation.

Conclusions:

  • Targeting foam cells is a validated therapeutic strategy in atherosclerosis.
  • Further research into disease-specific foam cell biology is essential.
  • Exploring therapeutic interventions targeting foam cells in other diseases holds potential.