Results 61 to 70 of about 1,126,451 (240)

Periostin‐CCL3 Feedforward Signaling Loop Promotes Cardiac Fibrosis and Cardiomyocyte Necroptosis in Arrhythmogenic Cardiomyopathy

Advanced Science, EarlyView.
POSTN‐CCL3 signaling forms a feed‐forward circuit between cardiomyocytes and cardiac myofibroblasts in arrhythmogenic cardiomyopathy. POSTN activates JNK/RIP3‐dependent necroptotic signaling and JNK/ETS2‐induced CCL3 expression in cardiomyocytes. In turn, CCL3‐CCR5 signaling in cardiac myofibroblasts activates NF‐κB/p65 and promotes POSTN expression ...
Tiantian Wu, Ruotong Li, Xiaoyue Zhang, Dandan Chen, Jianmeng Yang, Mengmeng Li, Yuhan Yin, Ya Wang, Yuqiu Tian, Haoling Yan, Dan Cui, Jiangping Song, Gaoliang Ouyang   +12 more
wiley   +1 more source

Benign masseter muscle hypertrophy

Brazilian Journal of Otorhinolaryngology, 2008
Summary: Idiopathic hypertrophy of the masseter muscle is a rare disorder of unknown cause. Some authors associate it with the habit of chewing gum, temporo-mandibular joint disorder, congenital and functional hypertrophies, and emotional disorders ...
Daniel Zeni Rispoli, Paulo M. Camargo, José L. Pires, Jr, Vinicius R. Fonseca, Karina K. Mandelli, Marcela A.C. Pereira   +5 more
doaj   +1 more source

Sarcoplasmic Hypertrophy in Skeletal Muscle: A Scientific “Unicorn” or Resistance Training Adaptation?

Frontiers in Physiology, 2020
Skeletal muscle fibers are multinucleated cells that contain mostly myofibrils suspended in an aqueous media termed the sarcoplasm. Select evidence suggests sarcoplasmic hypertrophy, or a disproportionate expansion of the sarcoplasm relative to myofibril
Michael D. Roberts, Michael D. Roberts, Cody T. Haun, Christopher G. Vann, Shelby C. Osburn, Kaelin C. Young, Kaelin C. Young   +6 more
doaj   +1 more source

Nuclear Translocation of PFKFB3 Promotes Disuse‐Induced Muscle Atrophy via Scaffolding Nedd4‐Mediated JunB Ubiquitination

Advanced Science, EarlyView.
Disuse‐induced muscle atrophy is driven by a non‐metabolic, nuclear function of the enzyme PFKFB3. Acting as a scaffold, PFKFB3 facilitates Nedd4‐mediated ubiquitination and degradation of the anti‐atrophy transcription factor JunB. Inhibiting this novel PFKFB3–Nedd4–JunB signaling axis stabilizes JunB and alleviates muscle wasting, revealing a highly ...
Mengjun Ma, Yinliang Liu, Wangchang Wu, Biao Yang, Jiahao Zhuang, Haoye Yu, Rujia Mi, Yixuan Lu, Wen Yang, Hanting Yi, Chenglong Yuan, Yinfeng Gu, Hongyu Li   +12 more
wiley   +1 more source

The Deubiquitinase UCHL1 Drives Susceptibility to Atrial Fibrillation by Stabilizing CaMKII‐δ

Advanced Science, EarlyView.
UCHL1 is highly upregulated in mice and patients with AF. UCHL1 directly binds to and removes K48‐linked polyubiquitin chains from CaMKII‐δ at K251 and enhances CaMKII‐δ stability, which activates RyR2, disrupts Ca2+ handling, and promotes AF. These findings establish UCHL1 as a critical regulator of CaMKII‐δ stability and AF‐related Ca2+ handling ...
Hai‐Lian Bi, Yu‐Hui Gu, Kai‐Wen Ren, Xiao‐Hong Yu, Yun‐Long Xia, Xiao‐Lei Yang, Hui‐Hua Li   +6 more
wiley   +1 more source

A Spatiotemporal Single‐Cell Atlas Uncovers Dysregulated ECM Dynamics and Septal Remodeling Arrest in Human Ventricular Septal Defects

Advanced Science, EarlyView.
Integrating single‐cell and spatial transcriptomics reveals human ventricular septal defect (VSD) as a disease of microenvironmental insufficiency and structural remodeling arrest. Attenuated endothelial‐fibroblast crosstalk, alongside downregulated THBS1/TGF‐β1 and MMP2 signaling networks, impairs the endothelial‐to‐mesenchymal transition (EndoMT) and
Xiaoyuan Zhang, Lun Zhu, Ze Sun, Ruolin Jia, Ziming Wang, Jiayao Zhao, Bohao Liu, Haiqing Xiong, Xiaowei Yu, Yanzhu Yue   +9 more
wiley   +1 more source

Myonuclear Domain Flexibility Challenges Rigid Assumptions on Satellite Cell Contribution to Skeletal Muscle Fiber Hypertrophy

Frontiers in Physiology, 2018
Satellite cell-mediated myonuclear accretion is thought to be required for skeletal muscle fiber hypertrophy, and even drive hypertrophy by preceding growth. Recent studies in humans and rodents provide evidence that challenge this axiom.
Kevin A. Murach, Kevin A. Murach, Davis A. Englund, Davis A. Englund, Esther E. Dupont-Versteegden, Esther E. Dupont-Versteegden, John J. McCarthy, John J. McCarthy, Charlotte A. Peterson, Charlotte A. Peterson   +9 more
doaj   +1 more source

Alkylating Agent–Induced FANCL Impairment Damages Pulmonary Arterial, Venous, and Microvascular Endothelial Cells and Predisposes to PAH/PVOD

Advanced Science, EarlyView.
This study establishes a novel cisplatin‐induced rat model of PAH/PVOD and identifies a conserved mechanistic axis—FANCL impairment, DNA damage accumulation, and endothelial dysfunction—triggered by cisplatin or mitomycin C across pulmonary arteries, veins, and microvessels.
Shiyun Liu, Yufei Sun, Xinlei Wu, Haixia Chen, Shaocong Mo, Zichong Li, Yiwei Gong, Xiaoqian Shan, Yuanqi Li, Yaru Guan, Junqi Zhu, Han Yan, Min Du, Feng Wei, Peixin Ou, Ziyi Wang, Chenting Zhang, Lei Xu, Wenju Lu, Jian Wang, Kai Yang   +20 more
wiley   +1 more source

Comparative transcriptomic analysis revealed potential mechanisms regulating the hypertrophy of goose pectoral muscles

Poultry Science
Pectoral muscle development is an important economic trait. According to the different essence, muscle development can be divided into 2 processes: embryonic muscle fiber generation and postnatal muscle fiber hypertrophy, and postnatal muscle fiber ...
Xinyue Hu, Yali Liu, Bincheng Tang, Jiwei Hu, Hua He, Hehe Liu, Liang Li, Shenqiang Hu, Jiwen Wang   +8 more
doaj   +1 more source

Do the anatomical and physiological properties of a muscle determine its adaptive response to different loading protocols?

Physiological Reports, 2020
It has been proposed that superior muscle hypertrophy may be obtained by training muscles predominant in type I fibers with lighter loads and those predominant in type II fibers with heavier loads.
Brad J. Schoenfeld, Andrew D. Vigotsky, Jozo Grgic, Cody Haun, Bret Contreras, Kenneth Delcastillo, Aston Francis, Gilda Cote, Andrew Alto   +8 more
doaj   +1 more source