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We are analyzing https://www.nature.com/articles/s41574-021-00551-9.

Title:
Autophagy in metabolic disease and ageing | Nature Reviews Endocrinology
Description:
Autophagy is an evolutionarily conserved, lysosome-dependent catabolic process whereby cytoplasmic components, including damaged organelles, protein aggregates and lipid droplets, are degraded and their components recycled. Autophagy has an essential role in maintaining cellular homeostasis in response to intracellular stress; however, the efficiency of autophagy declines with age and overnutrition can interfere with the autophagic process. Therefore, conditions such as sarcopenic obesity, insulin resistance and type 2 diabetes mellitus (T2DM) that are characterized by metabolic derangement and intracellular stresses (including oxidative stress, inflammation and endoplasmic reticulum stress) also involve the accumulation of damaged cellular components. These conditions are prevalent in ageing populations. For example, sarcopenia is an age-related loss of skeletal muscle mass and strength that is involved in the pathogenesis of both insulin resistance and T2DM, particularly in elderly people. Impairment of autophagy results in further aggravation of diabetes-related metabolic derangements in insulin target tissues, including the liver, skeletal muscle and adipose tissue, as well as in pancreatic β-cells. This Review summarizes the role of autophagy in the pathogenesis of metabolic diseases associated with or occurring in the context of ageing, including insulin resistance, T2DM and sarcopenic obesity, and describes its potential as a therapeutic target. The cellular consequences of dysfunctional autophagy contribute to numerous diseases. In this Review, Kitada and Koya consider the relationship between impaired autophagy and age-related metabolic derangements, including insulin resistance, type 2 diabetes mellitus and sarcopenic obesity, and discuss candidate autophagy-based therapies.
Website Age:
30 years and 10 months (reg. 1994-08-11).

Matching Content Categories {📚}

  • Education
  • Health & Fitness
  • Science

Content Management System {📝}

What CMS is nature.com built with?

Custom-built

No common CMS systems were detected on Nature.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of nature.com audience?

🌆 Monumental Traffic: 20M - 50M visitors per month


Based on our best estimate, this website will receive around 41,362,249 visitors per month in the current month.

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How Does Nature.com Make Money? {💸}


Display Ads {🎯}


The website utilizes display ads within its content to generate revenue. Check the next section for further revenue estimates.

Ads are managed by yourbow.com. Particular relationships are as follows:

Direct Advertisers (10)
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conversantmedia.com, rubiconproject.com, pubmatic.com, appnexus.com, openx.com, smartadserver.com, lijit.com, sharethrough.com, video.unrulymedia.com, google.com, yahoo.com, triplelift.com, onetag.com, sonobi.com, contextweb.com, 33across.com, indexexchange.com, media.net, themediagrid.com, adform.com, richaudience.com, sovrn.com, improvedigital.com, freewheel.tv, smaato.com, yieldmo.com, amxrtb.com, adyoulike.com, adpone.com, criteo.com, smilewanted.com, 152media.info, e-planning.net, smartyads.com, loopme.com, opera.com, mediafuse.com, betweendigital.com

How Much Does Nature.com Make? {💰}


Display Ads {🎯}

$521,200 per month
According to our algorithms, Nature.com's monthly online income from display advertising ranges from $347,485 to $955,583.

Keywords {🔍}

pubmed, article, google, scholar, cas, autophagy, central, cell, nature, diabetes, biol, nat, mice, sci, muscle, mol, cells, insulin, metabolic, stress, type, pancreatic, role, ampk, aging, autophagic, promotes, disease, lipid, obesity, skeletal, rep, metab, cellular, regulation, med, atg, ulk, commun, hepatic, content, resistance, restriction, access, metabolism, phosphorylation, function, ageing, koya, liver,

Topics {✒️}

medical research institute permissions reprints nature portfolio journals privacy policy nature portfolio editing advertising 5′-amp-activated protein kinase exercise-induced bcl2-regulated autophagy regional fat distribution social media author correspondence hypercaloric pro-diabetic regimens tfeb-regulated autophagy-lysosomal pathway palmitate-induced cellular senescence insulin/igf-1 receptor signaling collagen vi-deficient muscles mtor/p70s6k signaling pathway serine/threonine kinase ulk1 starvation-induced autoregulatory loop nad-dependent deacetylase sirt1 pancreatic β-cell death acyl-coa-binding protein acyl-coa binding protein mc3t3-e1 cells exposed acute exercise-induced autophagy dietary-induced obese mice hfd‑induced obese mice metabolic-stress-induced rearrangement tacrolimus-induced diabetes mellitus diet-induced obese mice sirt1-dependent mitochondrial autophagy diabetes-related metabolic derangements life-long exercise nutrient stress-induced autophagy rapamycin-induced insulin resistance nature+ nature 458 nature 432 nature 558 nature 510 nature 529 nature 481 nature 460 nature 425 nature 444 nature ampk-regulated 14-3-3ζ interaction lysosome-dependent catabolic process article content

Schema {🗺️}

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