MTMR7 suppresses the phenotypic switching of vascular smooth muscle cell and vascular intimal hyperplasia after injury via regulating p62/mTORC1-mediated glucose metabolism

Sun, Xiongshan; Yang, Yao; Zhao, Weiwei; Wang, Mingliang; Chen, Yingmei; Wang, Jia; Yang, Dachun; Yang, Yongjian

doi:10.1016/j.atherosclerosis.2024.117470

Cited by 3 publications

(1 citation statement)

References 42 publications

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“…Previous studies have found that MTMR7 is highly correlated with glucose metabolism and mammalian targets of rapamycin complex 1 (mTORC1). Further experiments confirmed that MTMR7 significantly inhibited glycolysis and mTORC1 activity in PDGF BB-excited VSMCs in vitro , so it was concluded that MTMR7 inhibited glucose metabolism and thus inhibited VSMC proliferation and migration and vascular intimal proliferation ( 61 ). PPARγ is a member of the nuclear receptor superfamily that plays a key role in the differentiation, maintenance, and function of adipocytes ( 62 ).…”

Section: Common Biological Functions Of Mtmrsmentioning

confidence: 93%

Recent advances of myotubularin-related (MTMR) protein family in cardiovascular diseases

Wang,

Guo,

Wang

et al. 2024

Front. Cardiovasc. Med.

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Belonging to a lipid phosphatase family containing 16 members, myotubularin-related proteins (MTMRs) are widely expressed in a variety of tissues and organs. MTMRs preferentially hydrolyzes phosphatidylinositol 3-monophosphate and phosphatidylinositol (3,5) bis-phosphate to generate phosphatidylinositol and phosphatidylinositol 5-monophosphate, respectively. These phosphoinositides (PIPs) promote membrane degradation during autophagosome-lysosomal fusion and are also involved in various regulatory signal transduction. Based on the ability of modulating the levels of these PIPs, MTMRs exert physiological functions such as vesicle trafficking, cell proliferation, differentiation, necrosis, cytoskeleton, and cell migration. It has recently been found that MTMRs are also involved in the occurrence and development of several cardiovascular diseases, including cardiomyocyte hypertrophy, proliferation of vascular smooth muscle cell, LQT1, aortic aneurysm, etc. This review summarizes the functions of MTMRs and highlights their pathophysiological roles in cardiovascular diseases.

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Section: Common Biological Functions Of Mtmrsmentioning

confidence: 93%

Recent advances of myotubularin-related (MTMR) protein family in cardiovascular diseases

Wang,

Guo,

Wang

et al. 2024

Front. Cardiovasc. Med.

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Silencing of <italic>PCK1</italic> mitigates the proliferation and migration of vascular smooth muscle cells and vascular intimal hyperplasia by suppressing STAT3/DRP1-mediated mitochondrial fission

Zhang,

Chen,

Pan

et al. 2024

ABBS

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Skeletal muscle-derived musclin attenuates glycolysis, oxidative stress, and pulmonary hypertension through the NPR3/AKT/mTORC1 pathway

Sun,

Wang,

Xiao

et al. 2024

ABBS

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MTMR7 suppresses the phenotypic switching of vascular smooth muscle cell and vascular intimal hyperplasia after injury via regulating p62/mTORC1-mediated glucose metabolism

Cited by 3 publications

References 42 publications

Recent advances of myotubularin-related (MTMR) protein family in cardiovascular diseases

Recent advances of myotubularin-related (MTMR) protein family in cardiovascular diseases

Silencing of <italic>PCK1</italic> mitigates the proliferation and migration of vascular smooth muscle cells and vascular intimal hyperplasia by suppressing STAT3/DRP1-mediated mitochondrial fission

Skeletal muscle-derived musclin attenuates glycolysis, oxidative stress, and pulmonary hypertension through the NPR3/AKT/mTORC1 pathway

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MTMR7 suppresses the phenotypic switching of vascular smooth muscle cell and vascular intimal hyperplasia after injury via regulating p62/mTORC1-mediated glucose metabolism

Cited by 3 publications

References 42 publications

Recent advances of myotubularin-related (MTMR) protein family in cardiovascular diseases

Recent advances of myotubularin-related (MTMR) protein family in cardiovascular diseases

Silencing of &lt;italic&gt;PCK1&lt;/italic&gt; mitigates the proliferation and migration of vascular smooth muscle cells and vascular intimal hyperplasia by suppressing STAT3/DRP1-mediated mitochondrial fission

Skeletal muscle-derived musclin attenuates glycolysis, oxidative stress, and pulmonary hypertension through the NPR3/AKT/mTORC1 pathway

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Product

Resources

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Silencing of <italic>PCK1</italic> mitigates the proliferation and migration of vascular smooth muscle cells and vascular intimal hyperplasia by suppressing STAT3/DRP1-mediated mitochondrial fission