Clinically distinguishable syndromes caused by viruses

Haynes, Ralph E.; Azimi, Parvin H.; Cramblett, Henry G.; Hilty, Milo D.; Burech, Dennis L.; Korányi, Katalin

doi:10.1016/s0045-9380(75)80017-x

Cited by 1 publication

(1 citation statement)

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“…Both the AF and NP serve in maintaining homeostasis of the spine; however, these components can degrade over time leading to what is clinically known as intervertebral disc degeneration [1]. IVD degeneration is a painful and progressive disease characterized by the breakdown of the IVD, causing hallmark signs of neck and back pain [4]. With neck and back pain being among the leading global causes of disability, understanding the pathophysiology of IVD degeneration paramount to restoring and preserving the functional lives of diagnosed patients.…”

Section: Introductionmentioning

confidence: 99%

Genetic Predictors of Early-Onset Spinal Intervertebral Disc Degeneration: Part One of Two

Covarrubias¹,

Jarrah²

2021

Cureus

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Intervertebral disc (IVD) degeneration is a progressive and painful pathology that can root from mechanical, biochemical, and environmental stressors. However, recent advancements in biogenetics have now found a predominating genetic influence. Nevertheless, despite these advancements, the pathophysiology of IVD degeneration remains poorly understood. In the first of our two-part series, we will characterize some of the most recent and best-studied genes in the context of intervertebral disc degeneration. We will attempt to formulate the first contemporary gene guide that characterizes the genetic profile of IVD degeneration. The genes of interest include aggrecan (ACAN), matrix metalloproteinase 2 (MMP2), vitamin D receptor (VDR), interleukin 1 alpha (IL1A), and those encoded for collagens such as collagen type XI alpha 1 chain (COL11A1), collagen type I alpha 1 chain (COL1A1), collagen type IX alpha 2 chain (COL9A2), and collagen type IX alpha 3 chain (COL9A3). Genetic analysis studies reveal that these genes play vital roles in maintaining the structural integrity of the intervertebral disc, activating enzymes involved in the extracellular matrix, and promoting connective tissue formation. Nevertheless, characterizing these genes alone is not enough to understand the pathophysiology of IVD degeneration. Therefore, further studies are warranted to understand molecular signalling pathways of IVD degeneration better and ultimately create more sophisticated genetic and cell-based therapies to improve patient outcomes.

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Section: Introductionmentioning

confidence: 99%