Could the kynurenine pathway be the key missing piece of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) complex puzzle?
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex and debilitating disease with a substantial social and economic impact on individuals and their community. Despite its importance and deteriorating impact, progresses in diagnosis and treatment of ME/CFS is limited. This is due...
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| Veröffentlicht in: | Cellular and molecular life sciences : CMLS 2022-08, Vol.79 (8), p.412-412, Article 412 |
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| creator | Kavyani, Bahar Lidbury, Brett A. Schloeffel, Richard Fisher, Paul R. Missailidis, Daniel Annesley, Sarah J. Dehhaghi, Mona Heng, Benjamin Guillemin, Gilles J. |
| description | Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex and debilitating disease with a substantial social and economic impact on individuals and their community. Despite its importance and deteriorating impact, progresses in diagnosis and treatment of ME/CFS is limited. This is due to the unclear pathophysiology of the disease and consequently lack of prognostic biomarkers. To investigate pathophysiology of ME/CFS, several potential pathologic hallmarks have been investigated; however, these studies have failed to report a consistent result. These failures in introducing the underlying reason for ME/CFS have stimulated considering other possible contributing mechanisms such as tryptophan (TRP) metabolism and in particular kynurenine pathway (KP). KP plays a central role in cellular energy production through the production of nicotinamide adenine dinucleotide (NADH). In addition, this pathway has been shown to mediate immune response and neuroinflammation through its metabolites. This review, we will discuss the pathology and management of ME/CFS and provide evidence pertaining KP abnormalities and symptoms that are classic characteristics of ME/CFS. Targeting the KP regulation may provide innovative approaches to the management of ME/CFS. |
| doi_str_mv | 10.1007/s00018-022-04380-5 |
| format | Article |
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Despite its importance and deteriorating impact, progresses in diagnosis and treatment of ME/CFS is limited. This is due to the unclear pathophysiology of the disease and consequently lack of prognostic biomarkers. To investigate pathophysiology of ME/CFS, several potential pathologic hallmarks have been investigated; however, these studies have failed to report a consistent result. These failures in introducing the underlying reason for ME/CFS have stimulated considering other possible contributing mechanisms such as tryptophan (TRP) metabolism and in particular kynurenine pathway (KP). KP plays a central role in cellular energy production through the production of nicotinamide adenine dinucleotide (NADH). In addition, this pathway has been shown to mediate immune response and neuroinflammation through its metabolites. This review, we will discuss the pathology and management of ME/CFS and provide evidence pertaining KP abnormalities and symptoms that are classic characteristics of ME/CFS. Targeting the KP regulation may provide innovative approaches to the management of ME/CFS.</description><identifier>ISSN: 1420-682X</identifier><identifier>EISSN: 1420-9071</identifier><identifier>DOI: 10.1007/s00018-022-04380-5</identifier><identifier>PMID: 35821534</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Abnormalities ; Adenine ; Biochemistry ; Biomarkers ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cellular manufacture ; Chronic fatigue syndrome ; Economic impact ; Encephalomyelitis ; Fatigue ; Fatigue Syndrome, Chronic - diagnosis ; Fatigue Syndrome, Chronic - therapy ; Humans ; Immune response ; Impact analysis ; Inflammation ; Kynurenine ; Life Sciences ; Metabolites ; NAD ; NADH ; Nicotinamide ; Nicotinamide adenine dinucleotide ; Pathophysiology ; Review ; Signs and symptoms ; Tryptophan</subject><ispartof>Cellular and molecular life sciences : CMLS, 2022-08, Vol.79 (8), p.412-412, Article 412</ispartof><rights>Crown 2022. corrected publication 2022</rights><rights>2022. 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Mol. Life Sci</addtitle><addtitle>Cell Mol Life Sci</addtitle><description>Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex and debilitating disease with a substantial social and economic impact on individuals and their community. Despite its importance and deteriorating impact, progresses in diagnosis and treatment of ME/CFS is limited. This is due to the unclear pathophysiology of the disease and consequently lack of prognostic biomarkers. To investigate pathophysiology of ME/CFS, several potential pathologic hallmarks have been investigated; however, these studies have failed to report a consistent result. These failures in introducing the underlying reason for ME/CFS have stimulated considering other possible contributing mechanisms such as tryptophan (TRP) metabolism and in particular kynurenine pathway (KP). KP plays a central role in cellular energy production through the production of nicotinamide adenine dinucleotide (NADH). 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Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kavyani, Bahar</au><au>Lidbury, Brett A.</au><au>Schloeffel, Richard</au><au>Fisher, Paul R.</au><au>Missailidis, Daniel</au><au>Annesley, Sarah J.</au><au>Dehhaghi, Mona</au><au>Heng, Benjamin</au><au>Guillemin, Gilles J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Could the kynurenine pathway be the key missing piece of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) complex puzzle?</atitle><jtitle>Cellular and molecular life sciences : CMLS</jtitle><stitle>Cell. Mol. Life Sci</stitle><addtitle>Cell Mol Life Sci</addtitle><date>2022-08-01</date><risdate>2022</risdate><volume>79</volume><issue>8</issue><spage>412</spage><epage>412</epage><pages>412-412</pages><artnum>412</artnum><issn>1420-682X</issn><eissn>1420-9071</eissn><abstract>Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex and debilitating disease with a substantial social and economic impact on individuals and their community. Despite its importance and deteriorating impact, progresses in diagnosis and treatment of ME/CFS is limited. This is due to the unclear pathophysiology of the disease and consequently lack of prognostic biomarkers. To investigate pathophysiology of ME/CFS, several potential pathologic hallmarks have been investigated; however, these studies have failed to report a consistent result. These failures in introducing the underlying reason for ME/CFS have stimulated considering other possible contributing mechanisms such as tryptophan (TRP) metabolism and in particular kynurenine pathway (KP). KP plays a central role in cellular energy production through the production of nicotinamide adenine dinucleotide (NADH). In addition, this pathway has been shown to mediate immune response and neuroinflammation through its metabolites. This review, we will discuss the pathology and management of ME/CFS and provide evidence pertaining KP abnormalities and symptoms that are classic characteristics of ME/CFS. 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| ispartof | Cellular and molecular life sciences : CMLS, 2022-08, Vol.79 (8), p.412-412, Article 412 |
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| subjects | Abnormalities Adenine Biochemistry Biomarkers Biomedical and Life Sciences Biomedicine Cell Biology Cellular manufacture Chronic fatigue syndrome Economic impact Encephalomyelitis Fatigue Fatigue Syndrome, Chronic - diagnosis Fatigue Syndrome, Chronic - therapy Humans Immune response Impact analysis Inflammation Kynurenine Life Sciences Metabolites NAD NADH Nicotinamide Nicotinamide adenine dinucleotide Pathophysiology Review Signs and symptoms Tryptophan |
| title | Could the kynurenine pathway be the key missing piece of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) complex puzzle? |
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