
Experimental and Molecular Pathology, Journal Year: 2025, Volume and Issue: 142, P. 104963 - 104963
Published: March 27, 2025
Language: Английский
Experimental and Molecular Pathology, Journal Year: 2025, Volume and Issue: 142, P. 104963 - 104963
Published: March 27, 2025
Language: Английский
Antioxidants, Journal Year: 2022, Volume and Issue: 11(9), P. 1686 - 1686
Published: Aug. 29, 2022
Various diseases can cause skeletal muscle atrophy, usually accompanied by inflammation, mitochondrial dysfunction, apoptosis, decreased protein synthesis, and enhanced proteolysis. The underlying mechanism of inflammation in atrophy is extremely complex has not been fully elucidated, thus hindering the development effective therapeutic drugs preventive measures for atrophy. In this review, we elaborate on degradation pathways, including ubiquitin-proteasome system (UPS), autophagy-lysosome pathway (ALP), calpain caspase insulin growth factor 1/Akt synthesis pathway, myostatin, satellite cells, process Under an inflammatory environment, various pro-inflammatory cytokines directly act nuclear factor-κB, p38MAPK, JAK/STAT pathways through corresponding receptors, then are involved Inflammation also indirectly trigger changing metabolic state other tissues or cells. This paper explores changes hypothalamic-pituitary-adrenal axis fat metabolism under conditions as well their effects muscle. Moreover, reviews signaling related to conditions, such cachexia, sepsis, type 2 diabetes mellitus, obesity, chronic obstructive pulmonary disease, kidney nerve injury. Finally, summarizes anti-amyotrophic targets recent years. Overall, a key causing anti-inflammation might be strategy treatment factors downstream considered promising prevention
Language: Английский
Citations
131Journal of Translational Medicine, Journal Year: 2023, Volume and Issue: 21(1)
Published: July 26, 2023
Abstract Mitochondria play important roles in maintaining cellular homeostasis and skeletal muscle health, damage to mitochondria can lead a series of pathophysiological changes. Mitochondrial dysfunction atrophy, its molecular mechanism leading atrophy is complex. Understanding the pathogenesis mitochondrial useful for prevention treatment finding drugs methods target modulate function are urgent tasks atrophy. In this review, we first discussed normal muscle. Importantly, described effect on mechanisms involved. Furthermore, regulatory different signaling pathways (AMPK-SIRT1-PGC-1α, IGF-1-PI3K-Akt-mTOR, FoxOs, JAK-STAT3, TGF-β-Smad2/3 NF-κB pathways, etc.) factors were investigated dysfunction. Next, analyzed manifestations caused by diseases. Finally, summarized preventive therapeutic effects targeted regulation including drug therapy, exercise diet, gene stem cell therapy physical therapy. This review great significance holistic understanding role muscle, which helpful researchers further has an inspiring development strategies targeting future.
Language: Английский
Citations
114Antioxidants, Journal Year: 2022, Volume and Issue: 12(1), P. 44 - 44
Published: Dec. 26, 2022
The maintenance of muscle homeostasis is vital for life and health. Skeletal atrophy not only seriously reduces people’s quality increases morbidity mortality, but also causes a huge socioeconomic burden. To date, no effective treatment has been developed skeletal owing to an incomplete understanding its molecular mechanisms. Exercise therapy the most atrophy. Unfortunately, it suitable all patients, such as fractured patients bedridden with nerve damage. Therefore, mechanism crucial developing new therapies In this review, PubMed was systematically screened articles that appeared in past 5 years about potential therapeutic strategies Herein, we summarize roles inflammation, oxidative stress, ubiquitin-proteasome system, autophagic-lysosomal pathway, caspases, calpains expound drug targets progress against This review focuses on current treatments atrophy, including (active substances traditional Chinese medicine, chemical drugs, antioxidants, enzyme inhibitors, hormone etc.), gene therapy, stem cell exosome (muscle-derived cells, non-myogenic exosomes), cytokine physical (electroacupuncture, electrical stimulation, optogenetic technology, heat low-level laser therapy), nutrition support (protein, essential amino acids, creatine, β-hydroxy-β-methylbutyrate, vitamin D), other (biomaterial adjuvant intestinal microbial regulation, oxygen supplementation). Considering many have propose combination proper individual needs, which may yield better outcomes.
Language: Английский
Citations
50Biochemical Pharmacology, Journal Year: 2022, Volume and Issue: 208, P. 115407 - 115407
Published: Dec. 31, 2022
Chronic kidney disease (CKD) is a high-risk chronic catabolic due to its high morbidity and mortality. CKD accompanied by many complications, leading poor quality of life, serious complications may even threaten the life patients. Muscle atrophy common complication CKD. sarcopenia in patients have complex pathways that are related multiple mechanisms factors. This review not only discusses which inflammation, oxidative stress, mitochondrial dysfunction promote CKD-induced muscle but also explores other CKD-related such as metabolic acidosis, vitamin D deficiency, anorexia, excess angiotensin II, well factors play role atrophy, insulin resistance, hormones, hemodialysis, uremic toxins, intestinal flora imbalance, miRNA. We highlight potential treatments drugs can effectively treat terms treatment, nutritional supplementation, physical exercise, drug intervention, thereby helping improve prognosis
Language: Английский
Citations
50Inflammopharmacology, Journal Year: 2024, Volume and Issue: 32(2), P. 1633 - 1646
Published: March 7, 2024
Language: Английский
Citations
9Cancer Cell International, Journal Year: 2024, Volume and Issue: 24(1)
Published: April 27, 2024
Abstract Triptolide (TPL) is a compound sourced from Tripterygium wilfordii Hook. F., traditional Chinese medicinal herb recognized for its impressive anti-inflammatory, anti-angiogenic, immunosuppressive, and antitumor qualities. Notwithstanding favorable attributes, the precise mechanism through which TPL influences tumor cells remains enigmatic. Its toxicity limited water solubility significantly impede clinical application of TPL. We offer comprehensive overview recent research endeavors aimed at unraveling in this review. Additionally, we briefly discuss current strategies to effectively manage challenges associated with future applications. By compiling information, aim enhance understanding underlying mechanisms involved identify potential avenues further advancement therapy.
Language: Английский
Citations
9International Immunopharmacology, Journal Year: 2023, Volume and Issue: 124, P. 111001 - 111001
Published: Oct. 5, 2023
Language: Английский
Citations
20Journal of Cachexia Sarcopenia and Muscle, Journal Year: 2023, Volume and Issue: 15(1), P. 173 - 188
Published: Nov. 27, 2023
Abstract Background Handelin is a bioactive compound from Chrysanthemum indicum L . that improves motor function and muscle integrity during aging in Caenorhabditis elegans This study aimed to further evaluate the protective effects molecular mechanisms of handelin mouse atrophy model induced by cachexia aging. Methods A tumour necrosis factor (TNF)‐α‐induced was used examine activity cultured C2C12 myotubes vitro Lipopolysaccharide (LPS)‐treated 8‐week‐old mice 23‐month‐old (aged) were therapeutic on cachexia‐ aging‐induced atrophy, respectively, vivo Protein mRNA expressions analysed Western blotting, ELISA quantitative PCR, respectively. Skeletal mass measured histological analysis. Results treatment resulted an upregulation protein levels early (MyoD myogenin) late (myosin heavy chain, MyHC) differentiation markers ( P < 0.05), enhanced mitochondrial respiratory 0.05). In TNF‐α‐induced myotube model, maintained MyHC levels, increased insulin‐like growth (Igf1 ) expression phosphorylated kinase B also reduced atrogin‐1 expression, inhibited nuclear factor‐κB activation interleukin Il 6 , Il1b chemokine ligand 1 Cxcl1 LPS‐treated mice, body weight 0.01) cross‐sectional area (CSA) soleus 0.0001) improved aged slightly tibialis anterior = 0.06) CSA gastrocnemius muscles 0.0001). upregulated Igf1 0.01), anti‐inflammatory cytokine Il10 biogenesis genes 0.05) antioxidant‐related enzymes strengthened Sod Cat enzyme lipid peroxidation carbonylation, downregulated Fbxo32 Mstn Tnf decreased IL‐1β serum Knockdown Hsp70 or using inhibitor abolished ameliorating atrophy. Conclusions ameliorated skeletal maintaining homeostasis synthesis degradation, possibly inhibiting inflammation. potentially promising drug candidate for wasting.
Language: Английский
Citations
18Molecular Nutrition & Food Research, Journal Year: 2024, Volume and Issue: 68(10)
Published: May 1, 2024
Abstract Skeletal muscle can undergo detrimental changes in various diseases, leading to dysfunction and atrophy, thus severely affecting people's lives. Along with exercise, there is a growing interest the potential of nutritional support against atrophy. This review provides brief overview molecular mechanisms driving skeletal atrophy summarizes recent advances interventions for preventing treating The supplements include amino acids their derivatives (such as leucine, β‐hydroxy, β‐methylbutyrate, creatine), antioxidant (like Coenzyme Q10 mitoquinone, resveratrol, curcumin, quercetin, Omega 3 fatty acids), minerals magnesium selenium), vitamins vitamin B, C, D, E), well probiotics prebiotics Lactobacillus, Bifidobacterium, 1‐kestose). Furthermore, study discusses impact combined approach involving physical therapy prevent suggests appropriate multi‐nutritional multi‐modal based on individual conditions optimize treatment outcomes, enhances recovery function patients. By understanding behind implementing interventions, it possible enhance improve patients' quality life.
Language: Английский
Citations
7Cells, Journal Year: 2022, Volume and Issue: 11(7), P. 1078 - 1078
Published: March 23, 2022
With global ageing, sarcopenia, as an age-related disease, has brought a heavy burden to individuals and society. Increasing attention been given further exploring the morbidity mechanism intervention measures for sarcopenia. Pyroptosis, also known cellular inflammatory necrosis, is kind of regulated cell death that plays role in ageing progress at level. It closely related diseases such cardiovascular diseases, Alzheimer’s osteoarthritis, In process aggravated oxidative stress poor skeletal muscle perfusion tissues can activate nod-like receptor (NLRP) family trigger pyroptosis. Chronic inflammation representative characteristic ageing. The levels factors TNF-α may signaling pathways pyroptosis by NF-κB-GSDMD axis, which remains be studied. Autophagy protective maintaining integrity intracellular organelles survival cells adverse conditions. autophagy inhibit activation pathway some extent. A profound understanding sarcopenia help identify new therapeutic targets future. This review article focuses on development progression
Language: Английский
Citations
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