Astaxanthin Supplementation Assists Sorafenib in Slowing Skeletal Muscle Atrophy in H22 Tumor‐Bearing Mice via Reversing Abnormal Glucose Metabolism DOI Open Access
Pengfei Ren, Xinyue Yu, Qingjuan Tang

et al.

Molecular Nutrition & Food Research, Journal Year: 2023, Volume and Issue: 67(16)

Published: May 13, 2023

Scope Cachexia, which is often marked by skeletal muscular atrophy, one of the leading causes death in cancer patients. Astaxanthin, a carotenoid obtained from marine organisms that can aid prevention and treatment variety disorders. In this study, to assess whether astaxanthin ameliorates weight loss muscle atrophy sorafenib‐treated hepatocellular carcinoma mice aimed. Methods results H22 are treated with 30 mg kg −1 day sorafenib 60 gavage lasted for 18 days. Sorafenib does not delay loss, although it reduce tumor burden. Astaxanthin dramatically delays sorafenib‐treating mice, without affecting food intake. inhibits glycolysis, slows down gluconeogenesis, improves insulin resistance tumor‐bearing mice. increases glucose competition targeting PI3K/Akt/GLUT4 signaling pathway, enhances utilization efficiency muscle, thereby slowing atrophy. Conclusion The findings show significant potential as nutritional supplements patients, well notion interventions should be implemented at initiation treatment, instead waiting until cachexia sets in.

Language: Английский

Short-chain fatty acids as potential regulators of skeletal muscle metabolism and function DOI
James E. Frampton, Kevin G. Murphy, Gary Frost

et al.

Nature Metabolism, Journal Year: 2020, Volume and Issue: 2(9), P. 840 - 848

Published: March 30, 2020

Language: Английский

Citations

321
The ubiquitin–proteasome system in regulation of the skeletal muscle homeostasis and atrophy: from basic science to disorders DOI Creative Commons
Yasuo Kitajima, Kiyoshi Yoshioka, Naoki Suzuki

et al.

The Journal of Physiological Sciences, Journal Year: 2020, Volume and Issue: 70(1)

Published: Sept. 16, 2020

Abstract Skeletal muscle is one of the most abundant and highly plastic tissues. The ubiquitin–proteasome system (UPS) recognised as a major intracellular protein degradation system, its function important for homeostasis health. Although UPS plays an essential role in during atrophy, leading to loss mass strength, deficit negatively impacts leads occurrence several pathological phenotypes. A growing number studies have linked impairment not only matured fibre degeneration weakness, but also stem cells deficiency regeneration. Emerging evidence suggests possible links between abnormal regulation types diseases. Therefore, understanding skeletal may provide novel therapeutic insights counteract wasting, various In this review, we focussed on proteasomes regeneration, including brief explanation structure proteasomes. addition, summarised recent findings diseases elaborated how related their states.

Language: Английский

Citations

117
Muscle-to-tumor crosstalk: The effect of exercise-induced myokine on cancer progression DOI

Qianrui Huang,

Meng‐Ling Wu,

Xuyi Wu

et al.

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, Journal Year: 2022, Volume and Issue: 1877(5), P. 188761 - 188761

Published: July 16, 2022

Language: Английский

Citations

56
Restoration of epigenetic impairment in the skeletal muscle and chronic inflammation resolution as a therapeutic approach in sarcopenia DOI
Gregory Livshits, Alexander Kalinkovich

Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 96, P. 102267 - 102267

Published: March 9, 2024

Language: Английский

Citations

13
The role of TGF-β signaling in muscle atrophy, sarcopenia and cancer cachexia DOI
Xinqiang Lan,

Chengjie Deng,

Qiquan Wang

et al.

General and Comparative Endocrinology, Journal Year: 2024, Volume and Issue: 353, P. 114513 - 114513

Published: April 10, 2024

Language: Английский

Citations

9
Ubiquitin Ligases at the Heart of Skeletal Muscle Atrophy Control DOI Creative Commons
Dulce Peris-Moreno, Laura Cussonneau, Lydie Combaret

et al.

Molecules, Journal Year: 2021, Volume and Issue: 26(2), P. 407 - 407

Published: Jan. 14, 2021

Skeletal muscle loss is a detrimental side-effect of numerous chronic diseases that dramatically increases mortality and morbidity. The alteration protein homeostasis generally due to increased breakdown while, synthesis may also be down-regulated. ubiquitin proteasome system (UPS) master regulator skeletal impacts contractile properties metabolism through multiple levers like signaling pathways, apparatus degradation, etc. Among the different actors UPS, E3 ligases specifically target key proteins for either degradation or activity modulation, thus controlling both pro-anabolic pro-catabolic factors. atrogenes MuRF1/TRIM63 MAFbx/Atrogin-1 encode respectively. However, several other are involved upstream in atrophy program, from signal transduction control modulation energy balance. Controlling tempting approach preserving mass. While indirect prove beneficial some situations atrophy, drugs directly inhibiting their have started appear. This review summarizes main pathways implicated, but molecules potentially usable future therapies.

Language: Английский

Citations

55
Altered glucose metabolism and insulin resistance in cancer-induced cachexia: a sweet poison DOI

Tamhida Masi,

Bhoomika M. Patel

Pharmacological Reports, Journal Year: 2020, Volume and Issue: 73(1), P. 17 - 30

Published: Nov. 3, 2020

Language: Английский

Citations

54
Chemotherapy-Induced Molecular Changes in Skeletal Muscle DOI Creative Commons
Mafalda Barbosa Pedrosa, Samuel Barbosa, Rui Vitorino

et al.

Biomedicines, Journal Year: 2023, Volume and Issue: 11(3), P. 905 - 905

Published: March 15, 2023

Paraneoplastic conditions such as cancer cachexia are often exacerbated by chemotherapy, which affects the patient’s quality of life well response to therapy. The aim this narrative review was overview body-composition-related changes and molecular effects different chemotherapy agents used in treatment on skeletal-muscle remodeling. A literature search performed using Web Science, Scopus, Science Direct databases a total 77 papers retrieved. In general, survey showed that induced skeletal muscle have been studied mainly animal models mostly non-tumor-bearing rodents, whereas clinical studies essentially assessed body composition computerized tomography. Data from preclinical modulates several pathways muscle, including ubiquitin–proteasome pathway, autophagy, IGF-1/PI3K/Akt/mTOR, IL-6/JAK/STAT, NF-κB pathway; however, newest underexplored. conclusion, exacerbates wasting patients; incomplete characterization chemotherapy-related makes development new preventive anti-wasting strategies difficult. Therefore, further investigation mechanisms necessary.

Language: Английский

Citations

18
ER Stress and Unfolded Protein Response in Cancer Cachexia DOI Open Access
Anirban Roy, Ashok Kumar

Cancers, Journal Year: 2019, Volume and Issue: 11(12), P. 1929 - 1929

Published: Dec. 3, 2019

Cancer cachexia is a devastating syndrome characterized by unintentional weight loss attributed to extensive skeletal muscle wasting. The pathogenesis of multifactorial because complex interactions tumor and host factors. irreversible wasting has been ascribed systemic inflammation, insulin resistance, dysfunctional mitochondria, oxidative stress, heightened activation ubiquitin-proteasome system macroautophagy. Accumulating evidence suggests that deviant regulation an array signaling pathways engenders cancer where the human body sustained in incessant self-consuming catabolic state. Recent studies have further suggested several components endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR) are activated animal models biopsies cachectic patients. However, exact role ER stress individual arms UPR mass various states including just begun be elucidated. This review provides succinct overview emerging roles cancer-induced

Language: Английский

Citations

47
Anabolic and Pro-metabolic Functions of CREB-CRTC in Skeletal Muscle: Advantages and Obstacles for Type 2 Diabetes and Cancer Cachexia DOI Creative Commons
Rebecca Berdeaux, Chase Hutchins

Frontiers in Endocrinology, Journal Year: 2019, Volume and Issue: 10

Published: Aug. 2, 2019

cAMP is one of the earliest described mediators hormone action in response to physiologic stress that allows acute responses and adaptation every tissue. The classic role signaling metabolic tissues regulate nutrient partitioning. In stress, such as epinephrine released during strenuous exercise or fasting, intramuscular liberates glucose from glycogen fatty acids triglycerides. long-term, activation Gs-coupled GPCRs stimulates muscle growth (hypertrophy) through multiple pathways culminate a net increase protein synthesis, mitochondrial biogenesis, improved efficiency. This review focuses on regulation, function transcriptional targets CREB (cAMP element binding protein) CRTCs (CREB regulated coactivators) skeletal potential for targeting this pathway sustain mass type 2 diabetes cancer. Although muscle-autonomous roles these proteins might render them excellent both conditions, pharmacologic must be approached with caution. Gain CREB-CRTC associated excess liver output diabetes, growing evidence implicates proliferation invasion different types cancer cells. We conclude deeper investigation identify specific regulatory mechanisms govern activity needed safely take advantage their potent effects invigorate potentially improve health people

Language: Английский

Citations

44