[Do Myokines Have Potential as Exercise Mimetics?]
Identifieur interne : 000198 ( Main/Exploration ); précédent : 000197; suivant : 000199[Do Myokines Have Potential as Exercise Mimetics?]
Auteurs : Yasuko ManabeSource :
- Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan [ 1347-5231 ] ; 2018.
Descripteurs français
- KwdFr :
- Découverte de médicament (MeSH), Développement musculaire (génétique), Développement musculaire (physiologie), Exercice physique (physiologie), Expression des gènes (MeSH), Facteurs inhibiteurs de la migration des macrophages (physiologie), Faiblesse musculaire (génétique), Faiblesse musculaire (traitement médicamenteux), Fibronectines (physiologie), Glutarédoxines (physiologie), Humains (MeSH), Interleukine-15 (physiologie), Interleukine-6 (physiologie), Muscles squelettiques (métabolisme), Myostatine (antagonistes et inhibiteurs), Myostatine (métabolisme), Myostatine (physiologie), Thiorédoxines (physiologie), Thérapie moléculaire ciblée (MeSH), Traitement par les exercices physiques (MeSH).
- MESH :
- antagonistes et inhibiteurs : Myostatine.
- génétique : Développement musculaire, Faiblesse musculaire.
- métabolisme : Muscles squelettiques, Myostatine.
- physiologie : Développement musculaire, Exercice physique, Facteurs inhibiteurs de la migration des macrophages, Fibronectines, Glutarédoxines, Interleukine-15, Interleukine-6, Myostatine, Thiorédoxines.
- traitement médicamenteux : Faiblesse musculaire.
- Découverte de médicament, Expression des gènes, Humains, Thérapie moléculaire ciblée, Traitement par les exercices physiques.
English descriptors
- KwdEn :
- Drug Discovery (MeSH), Exercise (physiology), Exercise Therapy (MeSH), Fibronectins (physiology), Gene Expression (MeSH), Glutaredoxins (physiology), Humans (MeSH), Interleukin-15 (physiology), Interleukin-6 (physiology), Macrophage Migration-Inhibitory Factors (physiology), Molecular Targeted Therapy (MeSH), Muscle Development (genetics), Muscle Development (physiology), Muscle Weakness (drug therapy), Muscle Weakness (genetics), Muscle, Skeletal (metabolism), Myostatin (antagonists & inhibitors), Myostatin (metabolism), Myostatin (physiology), Thioredoxins (physiology).
- MESH :
- chemical , antagonists & inhibitors : Myostatin.
- chemical , metabolism : Myostatin.
- chemical , physiology : Fibronectins, Glutaredoxins, Interleukin-15, Interleukin-6, Macrophage Migration-Inhibitory Factors, Myostatin, Thioredoxins.
- drug therapy : Muscle Weakness.
- genetics : Muscle Development, Muscle Weakness.
- metabolism : Muscle, Skeletal.
- physiology : Exercise, Muscle Development.
- Drug Discovery, Exercise Therapy, Gene Expression, Humans, Molecular Targeted Therapy.
Abstract
Exercise is generally considered to have health benefits for the body, although its beneficial mechanisms have not been fully elucidated. Recent progressive research suggests that myokines, bioactive substances secreted from skeletal muscle, play an important role in mediating the benefits of exercise. There are three types of myokines in terms of the muscular secretion mechanism: those in which the secretion is promoted by stimulation, such as irisin, interleukin (IL)-6, and IL-15; those whose secretion is constitutive, such as thioredoxin, glutaredoxin, and peroxiredoxin; and those whose secretion is suppressed by stimulation, such as by a macrophage migration inhibitory factor. Although dozens of myokines have been reported, their physiological roles are not well understood. Therefore, there currently exists no advanced drug discovery research specifically targeting myokines, with the exception of Myostatin. Myostatin was discovered as a negative regulator of muscle growth. Myostatin is secreted from muscle cells as a myokine; it signals via an activin type IIB receptor in an autocrine manner, and regulates gene expressions involved in myogenesis. Given the studies to date that have been conducted on the utilization of myostatin inhibitors for the treatment of muscle weakness, including cachexia and sarcopenia, other myokines may also be new potential drug targets.
DOI: 10.1248/yakushi.18-00091-5
PubMed: 30270273
Affiliations:
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(physiology)</term><term>Exercise Therapy (MeSH)</term><term>Fibronectins (physiology)</term><term>Gene Expression (MeSH)</term><term>Glutaredoxins (physiology)</term><term>Humans (MeSH)</term><term>Interleukin-15 (physiology)</term><term>Interleukin-6 (physiology)</term><term>Macrophage Migration-Inhibitory Factors (physiology)</term><term>Molecular Targeted Therapy (MeSH)</term><term>Muscle Development (genetics)</term><term>Muscle Development (physiology)</term><term>Muscle Weakness (drug therapy)</term><term>Muscle Weakness (genetics)</term><term>Muscle, Skeletal (metabolism)</term><term>Myostatin (antagonists & inhibitors)</term><term>Myostatin (metabolism)</term><term>Myostatin (physiology)</term><term>Thioredoxins (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Découverte de médicament (MeSH)</term><term>Développement musculaire (génétique)</term><term>Développement musculaire (physiologie)</term><term>Exercice physique (physiologie)</term><term>Expression des gènes (MeSH)</term><term>Facteurs inhibiteurs de la migration des macrophages (physiologie)</term><term>Faiblesse musculaire (génétique)</term><term>Faiblesse musculaire (traitement médicamenteux)</term><term>Fibronectines (physiologie)</term><term>Glutarédoxines (physiologie)</term><term>Humains (MeSH)</term><term>Interleukine-15 (physiologie)</term><term>Interleukine-6 (physiologie)</term><term>Muscles squelettiques (métabolisme)</term><term>Myostatine (antagonistes et inhibiteurs)</term><term>Myostatine (métabolisme)</term><term>Myostatine (physiologie)</term><term>Thiorédoxines (physiologie)</term><term>Thérapie moléculaire ciblée (MeSH)</term><term>Traitement par les exercices physiques (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Myostatin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" 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squelettiques</term><term>Myostatine</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Développement musculaire</term><term>Exercice physique</term><term>Facteurs inhibiteurs de la migration des macrophages</term><term>Fibronectines</term><term>Glutarédoxines</term><term>Interleukine-15</term><term>Interleukine-6</term><term>Myostatine</term><term>Thiorédoxines</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Exercise</term><term>Muscle Development</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Faiblesse musculaire</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Drug Discovery</term><term>Exercise Therapy</term><term>Gene Expression</term><term>Humans</term><term>Molecular Targeted Therapy</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Découverte de médicament</term><term>Expression des gènes</term><term>Humains</term><term>Thérapie moléculaire ciblée</term><term>Traitement par les exercices physiques</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"> Exercise is generally considered to have health benefits for the body, although its beneficial mechanisms have not been fully elucidated. Recent progressive research suggests that myokines, bioactive substances secreted from skeletal muscle, play an important role in mediating the benefits of exercise. There are three types of myokines in terms of the muscular secretion mechanism: those in which the secretion is promoted by stimulation, such as irisin, interleukin (IL)-6, and IL-15; those whose secretion is constitutive, such as thioredoxin, glutaredoxin, and peroxiredoxin; and those whose secretion is suppressed by stimulation, such as by a macrophage migration inhibitory factor. Although dozens of myokines have been reported, their physiological roles are not well understood. Therefore, there currently exists no advanced drug discovery research specifically targeting myokines, with the exception of Myostatin. Myostatin was discovered as a negative regulator of muscle growth. Myostatin is secreted from muscle cells as a myokine; it signals via an activin type IIB receptor in an autocrine manner, and regulates gene expressions involved in myogenesis. Given the studies to date that have been conducted on the utilization of myostatin inhibitors for the treatment of muscle weakness, including cachexia and sarcopenia, other myokines may also be new potential drug targets.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30270273</PMID><DateCompleted><Year>2018</Year><Month>10</Month><Day>19</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1347-5231</ISSN><JournalIssue CitedMedium="Internet"><Volume>138</Volume><Issue>10</Issue><PubDate><Year>2018</Year></PubDate></JournalIssue><Title>Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan</Title><ISOAbbreviation>Yakugaku Zasshi</ISOAbbreviation></Journal><ArticleTitle>[Do Myokines Have Potential as Exercise Mimetics?]</ArticleTitle><Pagination><MedlinePgn>1285-1290</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1248/yakushi.18-00091-5</ELocationID><Abstract><AbstractText> Exercise is generally considered to have health benefits for the body, although its beneficial mechanisms have not been fully elucidated. Recent progressive research suggests that myokines, bioactive substances secreted from skeletal muscle, play an important role in mediating the benefits of exercise. There are three types of myokines in terms of the muscular secretion mechanism: those in which the secretion is promoted by stimulation, such as irisin, interleukin (IL)-6, and IL-15; those whose secretion is constitutive, such as thioredoxin, glutaredoxin, and peroxiredoxin; and those whose secretion is suppressed by stimulation, such as by a macrophage migration inhibitory factor. Although dozens of myokines have been reported, their physiological roles are not well understood. Therefore, there currently exists no advanced drug discovery research specifically targeting myokines, with the exception of Myostatin. Myostatin was discovered as a negative regulator of muscle growth. Myostatin is secreted from muscle cells as a myokine; it signals via an activin type IIB receptor in an autocrine manner, and regulates gene expressions involved in myogenesis. Given the studies to date that have been conducted on the utilization of myostatin inhibitors for the treatment of muscle weakness, including cachexia and sarcopenia, other myokines may also be new potential drug targets.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Manabe</LastName><ForeName>Yasuko</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Health Promotion Sciences, Graduate School of Human Health Sciences, Tokyo Metropolitan University.</Affiliation></AffiliationInfo></Author></AuthorList><Language>jpn</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Japan</Country><MedlineTA>Yakugaku 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