A5022898250- Adipose Tissue and Metabolism
- Metabolism, Diabetes, and Cancer
- Muscle Physiology and Disorders
- Mitochondrial Function and Pathology
- Exercise and Physiological Responses
- Bone Metabolism and Diseases
- RNA modifications and cancer
- Endoplasmic Reticulum Stress and Disease
- Adipokines, Inflammation, and Metabolic Diseases
Model Animal Research Center
2020-2024
Nanjing Drum Tower Hospital
2020-2024
Nanjing University
2020-2023
Exercise-induced activation of adenosine monophosphate-activated protein kinase (AMPK) and substrate phosphorylation modulate the metabolic capacity mitochondria in skeletal muscle. However, key effector(s) AMPK regulatory mechanisms remain unclear. Here, we showed that folliculin interacting 1 (FNIP1) serine-220 (S220) controls mitochondrial function muscle fuel utilization during exercise. Loss FNIP1 resulted increased content augmented capacity, leading to enhanced exercise endurance...
Mitochondrial quality in skeletal muscle is crucial for maintaining energy homeostasis during metabolic stresses. However, how mitochondrial controlled and its physiological impacts remain unclear. Here, we demonstrate that mitoprotease LONP1 essential preserving proteostasis systemic homeostasis. Skeletal muscle-specific deletion of Lon protease homolog, (LONP1) impaired protein turnover, leading to stress. A benefit this adaptive response was the complete resistance diet-induced obesity....
Skeletal muscle depends on the precise orchestration of contractile and metabolic gene expression programs to direct fiber-type specification ensure performance. Exactly how such fiber type-specific patterns are established maintained remains unclear, however. Here, we demonstrate that histone monomethyl transferase MLL4 (KMT2D), an enhancer regulator enriched in slow myofibers, plays a critical role controlling identity as well muscle-specific ablation mice resulted downregulation oxidative...
Clinical evidence indicates a close association between muscle dysfunction and bone loss; however, the underlying mechanisms remain unclear. Here, we report that dysfunction–related loss in humans with limb-girdle muscular dystrophy is associated decreased expression of folliculin-interacting protein 1 (FNIP1) tissue. Supporting this finding, murine gain- loss-of-function genetic models demonstrated muscle-specific ablation FNIP1 caused mass, increased osteoclastic activity, mechanical...
Mitochondria are essential for maintaining skeletal muscle metabolic homeostasis during adaptive response to a myriad of physiologic or pathophysiological stresses. The mechanisms by which mitochondrial function and contractile fiber type concordantly regulated ensure remain poorly understood. Evidence is emerging that the Folliculin interacting protein 1 ( Fnip1 ) involved in specification, function, disease. In this study, was specifically expressed -transgenic Tg mice. mice were crossed...
Metabolically beneficial beige adipocytes offer tremendous potential to combat metabolic diseases. The folliculin interacting protein 1 (FNIP1) is implicated in controlling cellular metabolism via AMPK and mTORC1. However, whether how FNIP1 regulates adipocyte browning unclear. Here, we demonstrate that plays a critical role systemic glucose homeostasis. Adipocyte-specific ablation of promotes broad thermogenic remodeling adipocytes, including increased UCP1 levels, high mitochondrial...
Abstract Ischaemia of the heart and limbs attributable to compromised blood supply is a major cause mortality morbidity. The mechanisms functional angiogenesis remain poorly understood, however. Here we show that FNIP1 plays critical role in controlling skeletal muscle angiogenesis, process pivotal for revascularization during ischemia. Muscle expression down-regulated by exercise. Genetic overexpression myofiber causes limited mice, whereas its myofiber-specific ablation markedly promotes...
Skeletal muscle mitochondria are essential for maintaining metabolic homeostasis in response to a myriad of physiologic or pathophysiological stresses. The folliculin (FLCN)-interacting protein 1 (FNIP1) forms complex with AMP-activated kinase (AMPK), and we previously demonstrated that FNIP1 inhibits AMPK activity myocytes. Using gain- loss-of-function approaches mice, discovered is necessary, but not sufficient, suppress AMPK-dependent mitochondrial function skeletal muscle. Muscles...