Systematic Review: Models of Changes in Gene Expression of MTOR, MURF-1, and MAFBX in Rats and Mice

Crit Rev Eukaryot Gene Expr. 2020;30(1):57-75. doi: 10.1615/CritRevEukaryotGeneExpr.2020027491.

Abstract

Introduction: Various pathologies and lifestyle factors, such as nutritional factors and physical exercises, can alter the gene expression of proteins related to synthesis and degradation.

Aim: We performed a systematic review of atrophy models, cancer models, burn models, sepsis models, cardiac insufficiency models, amino acid supplementation models, protein supplementation models, and miscellaneous models that have altered the gene expression of MTOR, MURF-1, or MAFBX in rats and mice.

Materials and methods: We searched the literature in the following databases: Medline, Scielo.org, Scielo.br, Redib, Lilacs, and the Periodicos Capes.

Results: We selected 56 articles for this review.

Discussion: Several conditions can alter the gene expression of muscle proteins under conditions that stimulate muscle degradation pathways. Therefore, treatments must normalize the expression of the degradation pathways and potentiate the synthesis pathways so the muscular tissue confers an increase in functional capacity and thus, survival in diseased patients. Therefore, the reversal of the mechanisms that promote its depletion must be achieved.

Conclusion: Identification of the atrophic mechanisms present in pathologies and other conditions of muscular disuse in the scientific literature is fundamental for the adoption of clinical strategies to prevent protein degradation and to promote the maintenance and/or increase of muscle tissue. Such strategies include physical exercise, protein supplementation, and/or pharmacological applications, aimed toward restoring the fullness of functional capacity.

Publication types

  • Research Support, Non-U.S. Gov't
  • Systematic Review

MeSH terms

  • Amino Acid Metabolism, Inborn Errors / genetics
  • Amino Acid Metabolism, Inborn Errors / pathology
  • Animals
  • Arrhythmias, Cardiac / genetics
  • Arrhythmias, Cardiac / pathology
  • Atrophy / genetics
  • Atrophy / pathology
  • Burns / genetics
  • Burns / pathology
  • Disease Models, Animal
  • Gene Expression Regulation / genetics*
  • Humans
  • Mice
  • Muscle Proteins / genetics*
  • Neoplasms / genetics
  • Neoplasms / pathology
  • Rats
  • SKP Cullin F-Box Protein Ligases / genetics*
  • Sepsis / genetics
  • Sepsis / pathology
  • TOR Serine-Threonine Kinases / genetics*
  • Tripartite Motif Proteins / genetics*
  • Ubiquitin-Protein Ligases / genetics*

Substances

  • Muscle Proteins
  • Tripartite Motif Proteins
  • Fbxo32 protein, mouse
  • SKP Cullin F-Box Protein Ligases
  • Trim63 protein, rat
  • Ubiquitin-Protein Ligases
  • TOR Serine-Threonine Kinases
  • mTOR protein, mouse