162,177 research outputs found
Mammalian Target of Rapamycin Signaling in Cardiac Physiology and Disease
No full textThe protein kinase mammalian or mechanistic target of rapamycin (mTOR) is an atypical serine/threonine kinase that exerts its main cellular functions by interacting with specific adaptor proteins to form 2 different multiprotein complexes, mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). mTORC1 regulates protein synthesis, cell growth and proliferation, autophagy, cell metabolism, and stress responses, whereas mTORC2 seems to regulate cell survival and polarity. The mTOR pathway plays a key regulatory function in cardiovascular physiology and pathology. However, the majority of information available about mTOR function in the cardiovascular system is related to the role of mTORC1 in the unstressed and stressed heart. mTORC1 is required for embryonic cardiovascular development and for postnatal maintenance of cardiac structure and function. In addition, mTORC1 is necessary for cardiac adaptation to pressure overload and development of compensatory hypertrophy. However, partial and selective pharmacological and genetic inhibition of mTORC1 was shown to extend life span in mammals, reduce pathological hypertrophy and heart failure caused by increased load or genetic cardiomyopathies, reduce myocardial damage after acute and chronic myocardial infarction, and reduce cardiac derangements caused by metabolic disorders. The optimal therapeutic strategy to target mTORC1 and increase cardioprotection is under intense investigation. This article reviews the information available regarding the effects exerted by mTOR signaling in cardiovascular physiology and pathological states
Editorial commentary: How to implement research studies on extracellular vesicle administration in myocardial infarction
No full textMyocardial infarction (MI) remains one of the leading causes of death worldwide. Although treatments to reduce myocardial damage during MI are continuously improving, no therapy capable of remarkably inducing myocardial regeneration is currently avail- able for clinical use. For these reasons, a highly active area of re- search in the cardiovascular field is focused on the development of innovative therapies for cardiac repair after MI in order to reduce the subsequent incidence of heart failure (HF). Among the ap- proaches being studied, the potential beneficial pleiotropic effects elicited by extracellular vesicles (EVs) are particularly fascinating
[Report to Chief J. E. Curry, by an unknown author #1]
No full textReport to Chief J. E. Curry, by an unknown author. The report contains a list of officers who gave depositions to the United States Attorney
[Report to Chief J. E. Curry, by an unknown author #2]
No full textReport to Chief J. E. Curry, by an unknown author. The report contains a list of officers who gave depositions to the United States Attorney
Chelerythrine rapidly induces apoptosis through generation of reactive oxygen species in cardiac myocytes.
No full textBeta-adrenergic cardiac hypertrophy is mediated primarily by the beta(1)-subtype in the rat heart.
No full textHow to be young at heart? miR-22 as a potential therapeutic target to boost autophagy and protect the old myocardium
No full textChelerythrine rapidly induces apoptosis through generation of reactive oxygen species in cardiac myocytes.
No full textChelerythrine rapidly induces apoptosis through generation of reactive oxygen species in cardiac myocytes.
No full textBeta-adrenergic cardiac hypertrophy is mediated primarily by the beta(1)-subtype in the rat heart.
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