Ligamentum Flavum Fibrosis and Hypertrophy

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: 30 June 2025 | Viewed by 2250

Special Issue Editors


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Guest Editor
Ferguson Laboratory for Spine Research, Bethel Musculoskeletal Research Center, Department of Orthopaedic Surgery, University of Pittsburgh, Pittsburgh, PA 15219, USA
Interests: autophagy; aging; senescence; intervertebral disc; molecular biology; inflammation; immunometabolism

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Guest Editor
1. Ferguson Laboratory for Spine Research, Bethel Musculoskeletal Research Center, Department of Orthopaedic Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219, USA
2. McGowan Institute for Regenerative Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15219, USA
Interests: intervertebral disc; ligamentum flavum; tissue engineering; molecular biology; aging; pre-clinical models

Special Issue Information

Dear Colleagues, 

Hypertrophy of ligamentum flavum (HLF) is a common contributor to lumbar spinal stenosis (LSS) associated with low back pain. To date, there are no effective therapies for the prevention or treatment of HLF-related LSS. Laminectomies, i.e., surgical removal of the HLF, are among the most common procedures for relief of low back pain in patients over the age of 65. As the name suggests, fibrosis is a core pathological factor driving HLF; however, the mechanisms that promote HLF remain to be defined. The TGFb signaling pathway has long been implicated in the process of fibrosis, but there is now evidence that other cytokines and signaling pathways are also prominent contributors, including IL6, mitochondrial function, and ROS, as well as non-coding RNAs, among others. In addition, while chronic mechanical instability has long been considered a primary cause of HLF, the contributions of aging, genetics, environment, and systemic conditions are likely to play important roles in the disease. 

Today, there are a wide array of exciting molecular, cellular, and clinical diagnostic tools that are being applied to elucidate the etiology and pathophysiology of HLF. The forthcoming Special Issue on ligamentum flavum fibrosis and hypertrophy aims to provide a platform for researchers to contribute to and update the growing body of molecular, cellular, and clinical knowledge of this long understudied but common clinical condition. Therefore, submissions of literature reviews and original research articles covering studies related to any molecular, cellular, or clinical aspect of LF development, function, or disease (hypertrophy) are welcome, as are studies on therapy and cutting-edge clinical characterization and epidemiology.

Dr. Prashanta Silwal
Dr. Peter G. Alexander
Guest Editors

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Keywords

  • lumbar spinal stenosis
  • ligamentum flavum hypertophy
  • fibrosus
  • stem cells
  • cell signaling
  • immunoregulation
  • aging and senescence
  • magnetic resonance imaging

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Published Papers (1 paper)

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Review

26 pages, 1353 KiB  
Review
Cellular and Molecular Mechanisms of Hypertrophy of Ligamentum Flavum
by Prashanta Silwal, Allison M. Nguyen-Thai, Peter G. Alexander, Gwendolyn A. Sowa, Nam V. Vo and Joon Y. Lee
Biomolecules 2024, 14(10), 1277; https://doi.org/10.3390/biom14101277 - 10 Oct 2024
Cited by 1 | Viewed by 2073
Abstract
Hypertrophy of the ligamentum flavum (HLF) is a common contributor to lumbar spinal stenosis (LSS). Fibrosis is a core pathological factor of HLF resulting in degenerative LSS and associated low back pain. Although progress has been made in HLF research, the specific molecular [...] Read more.
Hypertrophy of the ligamentum flavum (HLF) is a common contributor to lumbar spinal stenosis (LSS). Fibrosis is a core pathological factor of HLF resulting in degenerative LSS and associated low back pain. Although progress has been made in HLF research, the specific molecular mechanisms that promote HLF remain to be defined. The molecular factors involved in the onset of HLF include increases in inflammatory cytokines such as transforming growth factor (TGF)-β, matrix metalloproteinases, and pro-fibrotic growth factors. In this review, we discuss the current understanding of the mechanisms involved in HLF with a particular emphasis on aging and mechanical stress. We also discuss in detail how several pathomechanisms such as fibrosis, proliferation and apoptosis, macrophage infiltration, and autophagy, in addition to several molecular pathways involving TGF-β1, mitogen-activated protein kinase (MAPKs), and nuclear factor-κB (NF-κB) signaling, PI3K/AKT signaling, Wnt signaling, micro-RNAs, extracellular matrix proteins, reactive oxygen species (ROS), etc. are involved in fibrosis leading to HLF. We also present a summary of the current advancements in preclinical animal models for HLF research. In addition, we update the current and potential therapeutic targets/agents against HLF. An improved understanding of the molecular processes behind HLF and a novel animal model are key to developing effective LSS prevention and treatment strategies. Full article
(This article belongs to the Special Issue Ligamentum Flavum Fibrosis and Hypertrophy)
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