The dichotomized role for acid sensing ion channels in musculoskeletal pain and inflammation

Sluka, Kathleen A.; Gregory, Nicholas S.

doi:10.1016/j.neuropharm.2014.12.013

Cited by 57 publications

(47 citation statements)

References 42 publications

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“…These data suggest decreases in pH can contribute to the generation of referred hyperalgesia and pain. Decreases in pH, protons, can activate acid sensing ion channels (ASICs) on the peripheral terminals of nociceptors (for review see Abdelhamid and Sluka, 2015, Sluka and Gregory, 2015). Indeed ASIC3 is located on sensory neurons, sensory neurons innervating skeletal muscle express more ASIC3 than those innervating the skin, and 80% of these ASIC3 positive skeletal muscle afferents co-express the nociceptive marker CGRP (Price et al, 2001, Molliver et al, 2005, Walder et al, 2011).…”

Section: Alterations In Nociceptors May Underlie Some Of the Pathologmentioning

confidence: 99%

Neurobiology of fibromyalgia and chronic widespread pain

2016

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Section: Alterations In Nociceptors May Underlie Some Of the Pathologmentioning

confidence: 99%

Neurobiology of fibromyalgia and chronic widespread pain

2016

Self Cite

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“…ASIC channels are found in both neuronal and non-neuronal tissues and are highly expressed in small nociceptive DRG neurons. Activation of ASIC channels in these neurons produces an excitatory depolarizing current and hypersensitive pain behavior (reviewed in [51]). The potential role of ASIC channels in pain physiology is illustrated by the effects of a number of toxins.…”

Section: Ion Channelsmentioning

confidence: 99%

Emerging Targets for the Management of Osteoarthritis Pain

Malfait

Miller

2016

Curr Osteoporos Rep

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Worldwide, osteoarthritis (OA) is one of the leading causes of chronic pain, for which adequate relief is not available. Ongoing peripheral input from the affected joint is a major factor in OA-associated pain. Therefore, this review focuses predominantly on peripheral targets emerging in the preclinical and clinical arena. Nerve growth factor is the most advanced of these targets, and its blockade has shown tremendous promise in clinical trials in knee OA. A number of different types of ion channels, including voltage-gated sodium channels and calcium channels, transient receptor potential channels and acid-sensing ion channels, are important for neuronal excitability and play a role in pain genesis. Few channel blockers have been tested in preclinical models of OA, with varying results. Finally, we discuss some examples of G-protein coupled receptors, which may offer attractive therapeutic strategies for OA pain, including receptors for bradykinin, calcitonin gene-related peptide, and chemokines. Since many of the pathways described above can be selectively and potently targeted, they offer an exciting opportunity for pain management in OA, either systemically or locally.

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“…One of them, importin α5, is colocalized with transcription factor STAT 3 and dynein . Pain is also mediated by acid‐sensing ion channels …”

Section: The Five Signs Of Inflammation: 2000 Years Latermentioning

confidence: 99%

“…287 Pain is also mediated by acid-sensing ion channels. 288 Fever is induced by exogenous and/or endogenous substances termed "pyrogens," such as the virulence factor of Gram-negative bacteria, LPS, also known as endotoxin, and cytokines, such as interleukin (IL)-1β. 289,290 The pyrogens are sensed by their cognate receptors on brain microvascular endothelial cells that form the neurovascular unit proximal to the brain thermoregulatory centre.…”

Section: Inflammation: 2000 Years Latermentioning

confidence: 99%

Decoding inflammation, its causes, genomic responses, and emerging countermeasures

Hawiger

Zienkiewicz

2019

Scand J Immunol

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Inflammation is the mechanism of diseases caused by microbial, autoimmune, allergic, metabolic and physical insults that produce distinct types of inflammatory responses. This aetiologic view of inflammation informs its classification based on a cause‐dependent mechanism as well as a cause‐directed therapy and prevention. The genomic era ushered in a new understanding of inflammation by highlighting the cell's nucleus as the centre of the inflammatory response. Exogenous or endogenous inflammatory insults evoke genomic responses in immune and non‐immune cells. These genomic responses depend on transcription factors, which switch on and off a myriad of inflammatory genes through their regulatory networks. We discuss the transcriptional paradigm of inflammation based on denying transcription factors’ access to the nucleus. We present two approaches that control proinflammatory signalling to the nucleus. The first approach constitutes a novel intracellular protein therapy with bioengineered physiologic suppressors of cytokine signalling. The second approach entails control of proinflammatory transcriptional cascades by targeting nuclear transport with a cell‐penetrating peptide that inhibits the expression of 23 out of the 26 mediators of inflammation along with the nine genes required for metabolic responses. We compare these emerging anti‐inflammatory countermeasures to current therapies. The transcriptional paradigm of inflammation offers nucleocentric strategies for microbial, autoimmune, metabolic, physical and other types of inflammation afflicting millions of people worldwide.

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The dichotomized role for acid sensing ion channels in musculoskeletal pain and inflammation

Cited by 57 publications

References 42 publications

Neurobiology of fibromyalgia and chronic widespread pain

Neurobiology of fibromyalgia and chronic widespread pain

Emerging Targets for the Management of Osteoarthritis Pain

Decoding inflammation, its causes, genomic responses, and emerging countermeasures

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