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Trimethylamine N-oxide: a meta-organismal axis linking the gut and fibrosis.
Jang, Jae Woong; Capaldi, Emma; Smith, Tracy; Verma, Priyanka; Varga, John; Ho, Karen J.
Afiliación
  • Jang JW; Department of Surgery, Feinberg School of Medicine, Northwestern University, 676 North St. Clair Street, Suite 650, Chicago, IL, 60611, USA.
  • Capaldi E; Department of Surgery, Feinberg School of Medicine, Northwestern University, 676 North St. Clair Street, Suite 650, Chicago, IL, 60611, USA.
  • Smith T; Department of Surgery, Feinberg School of Medicine, Northwestern University, 676 North St. Clair Street, Suite 650, Chicago, IL, 60611, USA.
  • Verma P; Department of Internal Medicine, University of Michigan, 1500 East Medical Center Drive, Floor 3, Reception A, Ann Arbor, MI, 48109, USA.
  • Varga J; Department of Internal Medicine, University of Michigan, 1500 East Medical Center Drive, Floor 3, Reception A, Ann Arbor, MI, 48109, USA.
  • Ho KJ; Department of Surgery, Feinberg School of Medicine, Northwestern University, 676 North St. Clair Street, Suite 650, Chicago, IL, 60611, USA. kho1@nm.org.
Mol Med ; 30(1): 128, 2024 Aug 23.
Article en En | MEDLINE | ID: mdl-39180015
ABSTRACT

BACKGROUND:

Tissue fibrosis is a common pathway to failure in many organ systems and is the cellular and molecular driver of myriad chronic diseases that are incompletely understood and lack effective treatment. Recent studies suggest that gut microbe-dependent metabolites might be involved in the initiation and progression of fibrosis in multiple organ systems. MAIN BODY OF THE MANUSCRIPT In a meta-organismal pathway that begins in the gut, gut microbiota convert dietary precursors such as choline, phosphatidylcholine, and L-carnitine into trimethylamine (TMA), which is absorbed and subsequently converted to trimethylamine N-oxide (TMAO) via the host enzyme flavin-containing monooxygenase 3 (FMO3) in the liver. Chronic exposure to elevated TMAO appears to be associated with vascular injury and enhanced fibrosis propensity in diverse conditions, including chronic kidney disease, heart failure, metabolic dysfunction-associated steatotic liver disease, and systemic sclerosis.

CONCLUSION:

Despite the high prevalence of fibrosis, little is known to date about the role of gut dysbiosis and of microbe-dependent metabolites in its pathogenesis. This review summarizes recent important advances in the understanding of the complex metabolism and functional role of TMAO in pathologic fibrosis and highlights unanswered questions.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Fibrosis / Microbioma Gastrointestinal / Metilaminas Límite: Animals / Humans Idioma: En Revista: Mol Med Asunto de la revista: BIOLOGIA MOLECULAR Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Fibrosis / Microbioma Gastrointestinal / Metilaminas Límite: Animals / Humans Idioma: En Revista: Mol Med Asunto de la revista: BIOLOGIA MOLECULAR Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido