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Book ChapterDOI

AMPK in Cardiovascular Diseases.

TLDR
The description of the multifaceted action of the two AMPK catalytic isoforms, α1 and α2, emphasizes the general protective action of this protein kinase against the development of critical pathologies like myocardial ischemia, cardiac hypertrophy, diabetic cardiomyopathy, and heart failure.
Abstract
This chapter summarizes the implication of AMP-activated protein kinase (AMPK) in the regulation of various physiological and pathological cellular events of great importance for the maintenance of cardiac function. These include the control of both metabolic and non-metabolic elements targeting the different cellular components of the cardiac tissue, i.e., cardiomyocytes, fibroblasts, and vascular cells. The description of the multifaceted action of the two AMPK catalytic isoforms, α1 and α2, emphasizes the general protective action of this protein kinase against the development of critical pathologies like myocardial ischemia, cardiac hypertrophy, diabetic cardiomyopathy, and heart failure.

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Journal ArticleDOI

AMP-Activated Protein Kinase: An Ubiquitous Signaling Pathway With Key Roles in the Cardiovascular System.

TL;DR: The role of AMPK in the cardiovascular system is discussed, including the molecular basis of mutations in AMPK that alter cardiac physiology and the proposed mechanisms by which AMPK regulates vascular function under physiological and pathophysiological conditions.
Journal ArticleDOI

AMP-Activated Protein Kinase Regulation of the NLRP3 Inflammasome during Aging

TL;DR: It is shown that several AMPK-dependent pathways regulate NLRP3 inflammasome activation during aging, suggestingNLRP3 as a potential pharmacological target in age-related diseases.
Journal ArticleDOI

NLRP3 inflammasome activation in inflammaging.

TL;DR: This work discusses the emerging concept that a key innate immune pathway, the NLRP3 inflammasome, is centrally involved in the recognition of triggers that appear during physiological aging and during metabolic stress and highlights potential strategies by which the detrimental inflammatory responses could be pharmacologically addressed.
Journal ArticleDOI

Small Extracellular Microvesicles Mediated Pathological Communications Between Dysfunctional Adipocytes and Cardiomyocytes as a Novel Mechanism Exacerbating Ischemia/Reperfusion Injury in Diabetic Mice

TL;DR: It is demonstrated for the first time that miR-130b-3p enrichment in dysfunctional adipocyte-derived sEV, and its suppression of multiple antiapoptotic/cardioprotective molecules in cardiomyocytes, is a novel mechanism exacerbating MI/R injury in the diabetic heart.
References
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Journal ArticleDOI

Prognostic Implications of Echocardiographically Determined Left Ventricular Mass in the Framingham Heart Study

TL;DR: The estimation of left ventricular mass by echocardiography offers prognostic information beyond that provided by the evaluation of traditional cardiovascular risk factors, and it is concluded that an increase in left Ventricular mass predicts a higher incidence of clinical events, including death, attributable to cardiovascular disease.
Journal ArticleDOI

AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1

TL;DR: A molecular mechanism for regulation of the mammalian autophagy-initiating kinase Ulk1, a homologue of yeast ATG1, is demonstrated and a signalling mechanism for UlK1 regulation and autophagic induction in response to nutrient signalling is revealed.
Journal ArticleDOI

TSC2 mediates cellular energy response to control cell growth and survival.

TL;DR: It is described that TSC2 is regulated by cellular energy levels and plays an essential role in the cellular energy response pathway and its phosphorylation by AMPK protect cells from energy deprivation-induced apoptosis.
Journal ArticleDOI

AMPK phosphorylation of raptor mediates a metabolic checkpoint.

TL;DR: AMPK directly phosphorylates the mTOR binding partner raptor on two well-conserved serine residues, and this phosphorylation induces 14-3-3 binding to raptor, uncovering a conserved effector of AMPK that mediates its role as a metabolic checkpoint coordinating cell growth with energy status.
Journal ArticleDOI

Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-beta.

TL;DR: It is shown that caspase-12 is localized to the ER and activated by ER stress, including disruption of ER calcium homeostasis and accumulation of excess proteins in ER, but not by membrane- or mitochondrial-targeted apoptotic signals, which may contribute to amyloid-β neurotoxicity.
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