Natural products, PGC-1 , and Duchenne muscular dystrophy.

Ipek Suntar; Antoni Sureda; Tarun Belwal; Ana Sanches Silva; Rosa Anna Vacca; Devesh Tewari; Eduardo Sobarzo-sánchez; Seyed Fazel Nabavi; Samira Shirooie; Ahmad Reza Dehpour; Suowen XU; Bahman Yousefi; Maryam Majidinia; Maria Daglia; Giuseppe D'antona; Seyed Mohammad Nabavi

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Natural products, PGC-1 , and Duchenne muscular dystrophy.

Author: Ipek SUNTAR ¹ ; Antoni SUREDA ² ; Tarun BELWAL ³ ; Ana SANCHES SILVA ⁴ ; Rosa Anna VACCA ⁵ ; Devesh TEWARI ⁶ ; Eduardo SOBARZO-SÁNCHEZ ⁷ ; Seyed Fazel NABAVI ⁸ ; Samira SHIROOIE ⁹ ; Ahmad Reza DEHPOUR ¹⁰ ; Suowen XU ¹¹ ; Bahman YOUSEFI ¹² ; Maryam MAJIDINIA ¹³ ; Maria DAGLIA ¹⁴ ; Giuseppe D'ANTONA ¹⁵ ; Seyed Mohammad NABAVI ⁸
Author Information

1. Department of Pharmacognosy, Faculty of Pharmacy, Gazi University, Etiler, Ankara 06330, Turkey.
2. Research Group in Community Nutrition and Oxidative Stress, Health Research Institute of the Balearic Islands (IdISBa), and CIBEROBN (Physiopathology of Obesity and Nutrition), University of Balearic Islands, Palma, Balearic Islands E-07122, Spain.
3. G. B. Pant National Institute of Himalayan Environment and Sustainable Development, Kosi-Katarmal, Almora, Uttarakhand 263643, India.
4. National Institute for Agricultural and Veterinary Research (INIAV), Vairão, Vila do Conde, Portugal.
5. Institute of Biomembranes, Bioenergetics and Molecular Biotechnologies, National Council of Research, Bari 70126, Italy.
6. Department of Pharmacognosy, School of Pharmaceutical Sciences, Lovely Professional University, Phagwara, Punjab 144411, India.
7. Laboratory of Pharmaceutical Chemistry, Faculty of Pharmacy, University of Santiago de Compostela, Santiago de Compostela 15782, Spain.
8. Applied Biotechnology Research Center, Baqiyatallah University of Medical Sciences, Tehran 5613156491, Iran.
9. Pharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah 6715847141, Iran.
10. Department of Pharmacology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran 1416753955, Iran.
11. The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230001, China.
12. Molecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz 516615731, Iran.
13. Solid Tumor Research Center, Urmia University of Medical Sciences, Urmia 571478334, Iran.
14. Department of Pharmacy, University of Naples Federico II, Naples 80138, Italy.
15. Department of Public Health, Experimental and Forensic Medicine and CRIAMS-Sport Medicine Centre, University of Pavia, Pavia 27100, Italy.
Publication Type:Journal Article
Keywords: AAV, adeno-associated virus; AMP, adenosine monophosphate; AMPK, 5′ adenosine monophosphate-activated protein kinase; ASO, antisense oligonucleotides; ATF2, activating transcription factor 2; ATP, adenosine triphosphate; BMD, Becker muscular dystrophy; COPD, chronic obstructive pulmonary disease; CREB, cyclic AMP response element-binding protein; CnA, calcineurin a; DAGC, dystrophin-associated glycoprotein complex; DGC, dystrophin–glycoprotein complex; DMD, Duchenne muscular dystrophy; DRP1, dynamin-related protein 1; DS, Down syndrome; ECM, extracellular matrix; EGCG, epigallocatechin-3-gallate; ERRα, estrogen-related receptor alpha; FDA, U. S. Food and Drug Administration; FGF, fibroblast growth factor; FOXO1, forkhead box class-O1; GABP, GA-binding protein; GPX, glutathione peroxidase; GSK3b, glycogen synthase kinase 3b; HCT, hydrochlorothiazide; HDAC, histone deacetylase; HIF-1α, hypoxia-inducible factors; IL, interleukin; LDH, lactate dehydrogenase; MCP-1, monocyte chemoattractant protein-1; MD, muscular dystrophy; MEF2, myocyte enhancer factor 2; MSCs, mesenchymal stem cells; Mitochondrial oxidative phosphorylation; Muscular dystrophy; MyoD, myogenic differentiation; NADPH, nicotinamide adenine dinucleotide phosphate; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; NMJ, neuromuscular junctions; NO, nitric oxide; NOS, NO synthase; Natural product; PDGF, platelet derived growth factor; PGC-1, peroxisome proliferator-activated receptor γ coactivator 1; PPARγ activation; PPARγ, peroxisome proliferator-activated receptor γ; Peroxisome proliferator-activated receptor γ coactivator 1α; ROS, reactive oxygen species; Reactive oxygen species; SIRT1, silent mating type information regulation 2 homolog 1; SOD, superoxide dismutase; SPP1, secreted phosphoprotein 1; TNF-α, tumor necrosis factor-α; UCP, uncoupling protein; VEGF, vascular endothelial growth factor; cGMP, cyclic guanosine monophosphate; iPSCs, induced pluripotent stem cells; p38 MAPK, p38 mitogen-activated protein kinase
From: Acta Pharmaceutica Sinica B 2020;10(5):734-745
CountryChina
Language:English
Abstract: Peroxisome proliferator-activated receptor (PPAR) is a transcriptional coactivator that binds to a diverse range of transcription factors. PPAR coactivator 1 (PGC-1) coactivators possess an extensive range of biological effects in different tissues, and play a key part in the regulation of the oxidative metabolism, consequently modulating the production of reactive oxygen species, autophagy, and mitochondrial biogenesis. Owing to these findings, a large body of studies, aiming to establish the role of PGC-1 in the neuromuscular system, has shown that PGC-1 could be a promising target for therapies targeting neuromuscular diseases. Among these, some evidence has shown that various signaling pathways linked to PGC-1 are deregulated in muscular dystrophy, leading to a reduced capacity for mitochondrial oxidative phosphorylation and increased reactive oxygen species (ROS) production. In the light of these results, any intervention aimed at activating PGC-1 could contribute towards ameliorating the progression of muscular dystrophies. PGC-1 is influenced by different patho-physiological/pharmacological stimuli. Natural products have been reported to display modulatory effects on PPAR activation with fewer side effects in comparison to synthetic drugs. Taken together, this review summarizes the current knowledge on Duchenne muscular dystrophy, focusing on the potential effects of natural compounds, acting as regulators of PGC-1.