Article
Biochemistry & Molecular Biology
Luz Marina Sanchez-Mendoza, Carlos Perez-Sanchez, Sandra Rodriguez-Lopez, Chary Lopez-Pedrera, Miguel Calvo-Rubio, Rafael de Cabo, Maria I. Buron, Jose A. Gonzalez-Reyes, Jose M. Villalba
Summary: The study investigates the effect of sex on metabolic adaptations induced by overexpression of CYB5R3 and the modulation of key markers related to mitochondrial function in skeletal muscle. It was found that CYB5R3 overexpression leads to enhanced mitochondrial biogenesis and function, as well as increased mitochondrial abundance in skeletal muscle. These beneficial actions are predominantly observed in females, with differences in NADH levels and the abundance of cytochrome c and DRP-1. The results also show ultrastructural changes in transgenic females, including an increase in the number and size of mitochondria.
FREE RADICAL BIOLOGY AND MEDICINE
(2023)
Article
Biochemistry & Molecular Biology
Eun Ju Lee, Sibhghatulla Shaikh, Mohammad Hassan Baig, So-Young Park, Jeong Ho Lim, Syed Sayeed Ahmad, Shahid Ali, Khurshid Ahmad, Inho Choi
Summary: This study reports the potential of novel peptides MIF1 and MIF2 derived from MSTN in enhancing myogenesis and reducing adipogenesis. Modified MIF1 and MIF2 showed better cell proliferation and differentiation compared to non-modified peptides. Pretreatment of mice with (Ac)-MIF1 or (Ac)-MIF2-(NH2) promoted muscle regeneration.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Biochemistry & Molecular Biology
Siegfried Labeit, Stephanie Hirner, Julijus Bogomolovas, Andre Cruz, Moldir Myrzabekova, Anselmo Moriscot, Thomas Scott Bowen, Volker Adams
Summary: The muscle-specific ubiquitin ligase MuRF1 is involved in regulating muscle catabolism during chronic wasting states, with potential implications for glucose and fat metabolism regulation. Knockout mice for MuRF1 and MuRF2 show elevated serum glucose, triglycerides, and perturbed signaling pathways related to glucose and fat metabolism. Adenoviral re-expression of MuRF1 in KO mice helps normalize metabolic parameters, while the inhibitors MyoMed-205 and MyoMed-946 show potential in attenuating muscle weakness in a mouse model for T2DM.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Biochemistry & Molecular Biology
Ichiro Yamauchi, Yoriko Sakane, Takafumi Yamashita, Takuro Hakata, Taku Sugawa, Haruka Fujita, Kentaro Okamoto, Daisuke Taura, Keisho Hirota, Yohei Ueda, Toshihito Fujii, Akihiro Yasoda, Nobuya Inagaki
Summary: This study aimed to investigate the effects of peripheral iodothyronine deiodinases (DIOs) on thyroid hormone economy. The results showed that D2 could enhance local thyroid hormone action and promote its circulation, while D3 could decrease circulating T3 and T4 levels with elevated reverse T3, leading to consumptive hypothyroidism. Additionally, the D3 mice are expected to be a novel hypothyroidism model.
Article
Geriatrics & Gerontology
Volker Adams, Antje Schauer, Antje Augstein, Virginia Kirchhoff, Runa Draskowski, Anett Jannasch, Keita Goto, Gemma Lyall, Anita Maennel, Peggy Barthel, Norman Mangner, Ephraim B. Winzer, Axel Linke, Siegfried Labeit
Summary: MyoMed-205 improved myocardial diastolic function and prevented SKM atrophy/function in the HFpEF animal model. Mechanistically, SKM benefited from attenuation of the ubiquitin proteasome system and increased synthesis/activity of proteins of the mitochondrial respiratory chain, while the myocardium benefited from reduced titin modifications and fibrosis.
JOURNAL OF CACHEXIA SARCOPENIA AND MUSCLE
(2022)
Article
Multidisciplinary Sciences
Margarita Beckerman, Chava Harel, Inbal Michael, Amira Klip, Philip J. Bilan, Emily J. Gallagher, Derek LeRoith, Eli C. Lewis, Eddy Karnieli, Shulamit Levenberg
Summary: The study successfully demonstrated that engineered muscle constructs composed of GLUT4-overexpressing cells can effectively reduce and stabilize basal glucose levels in diabetic mice, suggesting a potential innovative modality for T2D therapy.
Article
Oncology
Yang Yang, Xuege Yang, Yating Huang, Sujuan Liu, Yanmei Niu, Li Fu
Summary: This study investigated the protective effects of resistance exercise in dexamethasone-induced muscle atrophy and found that Sestrin2 plays a vital role in this process. Resistance exercise increased Sestrin2 expression, which improved muscle atrophy by inhibiting the activation of the ubiquitin-proteasome pathway and MSTN/Smad signaling pathways.
EXPERIMENTAL CELL RESEARCH
(2023)
Article
Biochemistry & Molecular Biology
Marta Tomczyk, Alicja Braczko, Patrycja Jablonska, Adriana Mika, Kamil Przyborowski, Agata Jedrzejewska, Oliwia Krol, Filip Kus, Tomasz Sledzinski, Stefan Chlopicki, Ewa M. Slominska, Ryszard T. Smolenski
Summary: Dyslipidemia is often associated with skeletal muscle dysfunction, but research has shown in some mice an improvement in exercise capacity. This is achieved through increased mitochondria numbers, enhanced muscle strength, and promotion of fatty acid oxidation. Importantly, Ranolazine-mediated inhibition of FFA oxidation leads to reduced exercise capacity.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Multidisciplinary Sciences
Takayuki Ozawa, Masato Morikawa, Yasuyuki Morishita, Kazuki Ogikubo, Fumiko Itoh, Daizo Koinuma, Per-Ake Nygren, Kohei Miyazono
Summary: Targeting the signaling pathway of GDF8 is considered a promising strategy to increase muscle mass, with FSTL3 being an endogenous antagonist that can neutralize activin, GDF8, and GDF11. The use of monovalent FSTL3-Fc has shown to effectively promote muscle growth, overcoming challenges faced by current anti-GDF8 therapies.
Review
Cell Biology
Ming-Ming Chen, Yi-Ping Zhao, Yue Zhao, Shou-Long Deng, Kun Yu
Summary: Myostatin, a member of the TGF-β superfamily, negatively regulates skeletal muscle growth and development through autocrine or paracrine signaling, with mutations leading to increased muscle mass. It regulates myogenic differentiation, protein synthesis, and oxidative stress in skeletal muscle.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Shinsuke Tamai, Shin-ichiro Fujita, Ritsuko Komine, Yasuharu Kanki, Kai Aoki, Koichi Watanabe, Kazuhiro Takekoshi, Takehito Sugasawa
Summary: This study investigated the effects of cryotherapy on skeletal muscle using zebrafish as an animal model. The findings suggest that acute cold exposure transiently upregulates E3 ubiquitin ligases, especially MuRF1, indicating that cryotherapy may contribute to the treatment of trauma or fatigue by promoting protein processing.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2022)
Article
Biochemistry & Molecular Biology
Bing Fu, Jinzeng Yang, Yan Yang, Jun Xia, Yinglin He, Qing Wang, Huihong Zhao, Huirong Yang
Summary: This study investigated the role of myostatin in E. coioides and demonstrated the positive effects of autologous nucleic acid vaccine on muscle growth.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Physiology
Caroline Barbe, Audrey Loumaye, Pascale Lause, Olli Ritvos, Jean-Paul Thissen
Summary: Myostatin, a negative regulator of muscle development, inhibits muscle growth and requires activation of specific signaling pathways. Pak1 has been identified as a potential mediator of Myostatin action on skeletal muscle mass, playing a permissive role in the skeletal muscle mass increase caused by Myostatin inhibition.
FRONTIERS IN PHYSIOLOGY
(2021)
Article
Multidisciplinary Sciences
Andrew Norton, Kathleen Thieu, Cory W. Baumann, Dawn A. Lowe, Kim C. Mansky
Summary: Osteoporosis and sarcopenia are more prevalent in women as they age. Recent research has shown that estrogen signaling has an impact on the chemical communication between bone and muscle cells, and a deficiency in estrogen can lead to increased expression of myokines, which further accelerates bone loss in women.
SCIENTIFIC REPORTS
(2022)
Article
Cell Biology
Eun Ju Lee, Syed Sayeed Ahmad, Jeong Ho Lim, Khurshid Ahmad, Sibhghatulla Shaikh, Yun-Sil Lee, Sang Joon Park, Jun O. Jin, Yong-Ho Lee, Inho Choi
Summary: The study found that FMOD inhibits muscle aging by negatively regulating MSTN gene expression or suppressing MSTN protein, while MSTN promotes muscle aging by positively regulating the expressions of Atrogin1, CD36, and PPAR gamma genes in muscle.