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Lymphedema: From Mechanism to Treatment

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 October 2025 | Viewed by 1429

Special Issue Editor


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Guest Editor
I2MC, Université de Toulouse, Inserm UMR 1297, UT3, Toulouse, France
Interests: lymphatic vessels; lymphedema; extracellular matrix; fibrosis; vessel on-chip; collagen crosslinking

Special Issue Information

Dear Colleagues,

Lymphedema, characterized by chronic swelling due to lymphatic system dysfunction, poses significant clinical challenges. This comprehensive review invites original research and insightful reviews exploring the multifaceted nature of lymphedema, from underlying mechanisms to innovative treatment approaches. We seek contributions that elucidate the molecular, cellular, and genetic mechanisms of lymphatic disorders, advancements in diagnostic imaging, and biomarkers for early detection. As lymphedema is increasingly being recognized as a multifactorial condition, we emphasize the importance of studies that consider the multifactorial nature of lymphedema, particularly the roles of inflammation, adipose tissue accumulation, and fibrosis in disease progression and treatment response. Papers addressing novel therapeutic interventions, including surgical techniques and pharmacological treatments, are highly encouraged. Our goal is to create a multidisciplinary dialogue that bridges basic research and clinical practice, fostering collaborations that accelerate the translation of scientific discoveries into effective patient care. By contributing to this Special Issue, researchers can highlight their work’s significance and engage with a global community dedicated to improving lymphedema outcomes.

Dr. Florent Morfoisse
Guest Editor

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Keywords

  • lymphedema
  • lymphatic dysfunction
  • molecular mechanisms
  • cell signaling
  • diagnostic imaging
  • biomarkers
  • therapeutic interventions
  • inflammation
  • adipose tissue accumulation
  • fibrosis

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Published Papers (1 paper)

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Research

14 pages, 4642 KiB  
Article
Dynamics of Immune Cell Infiltration and Fibroblast-Derived IL-33/ST2 Axis Induction in a Mouse Model of Post-Surgical Lymphedema
by Kazuhisa Uemura, Kei-ichi Katayama, Toshihiko Nishioka, Hikaru Watanabe, Gen Yamada, Norimitsu Inoue and Shinichi Asamura
Int. J. Mol. Sci. 2025, 26(3), 1371; https://doi.org/10.3390/ijms26031371 - 6 Feb 2025
Viewed by 863
Abstract
Lymphedema is an intractable disease most commonly associated with lymph node dissection for cancer treatment and can lead to a decreased quality of life. Type 2 T helper (Th2) lymphocytes have been shown to be important in the progression of lymphedema. The activation [...] Read more.
Lymphedema is an intractable disease most commonly associated with lymph node dissection for cancer treatment and can lead to a decreased quality of life. Type 2 T helper (Th2) lymphocytes have been shown to be important in the progression of lymphedema. The activation of IL-33 and its receptor, the suppression of tumorigenicity 2 (ST2) signaling pathway, induces the differentiation of Th2 cells, but its involvement in lymphedema remains unclear. In the present study, we analyzed the dynamics of immune cell infiltration, including the IL-33/ST2 axis, in a mouse tail lymphedema model. Neutrophil infiltration was first detected in the lymphedema tissue on postoperative day (POD) 2. Macrophage infiltration increased from POD 2 to 5. The number of CD4+ T cells, including 50% Tregs, gradually increased from POD 14. The mRNA expression of ll13 and Ifng increased on POD 21. The expression of IL-33 was induced in fibroblast nuclei within dermal and subcutaneous tissues from POD 2, and the expression of the Il1rl1 gene encoding ST2 increased from POD 7. We demonstrated the infiltration process from innate to acquired immune cells through the development of a mouse tail lymphedema. The IL-33/ST2 axis was found to be induced during the transition from innate to acquired immunity. Full article
(This article belongs to the Special Issue Lymphedema: From Mechanism to Treatment)
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