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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
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We are analyzing https://link.springer.com/article/10.1007/s10522-024-10153-3.

Title:
Aging, ROS, and cellular senescence: a trilogy in the progression of liver fibrosis | Biogerontology
Description:
Ageing is an inevitable and multifaceted biological process that impacts a wide range of cellular and molecular mechanisms, leading to the development of various diseases, such as liver fibrosis. Liver fibrosis progresses to cirrhosis, which is an advanced form due to high amounts of extracellular matrix and restoration of normal liver structure with failure to repair damaged tissue and cells, marking the end of liver function and total liver failure, ultimately death. The most important factors are reactive oxygen species (ROS) and cellular senescence. Oxidative stress is defined as an impairment by ROS, which are by-products of the mitochondrial electron transport chain and other key molecular pathways that induce cell damage and can activate cellular senescence pathways. Cellular senescence is characterized by pro-inflammatory cytokines, growth factors, and proteases secreted by senescent cells, collectively known as the senescence-associated secretory phenotype (SASP). The presence of senescent cells, which disrupt tissue architecture and function and increase senescent cell production in liver tissues, contributes to fibrogenesis. Hepatic stellate cells (HSCs) are activated in response to chronic liver injury, oxidative stress, and senescence signals that drive excessive production and deposition of extracellular matrix. This review article aims to provide a comprehensive overview of the pathogenic role of ROS and cellular senescence in the aging liver and their contribution to fibrosis.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Health & Fitness
  • Science

Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

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

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

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How Does Link.springer.com Make Money? {πŸ’Έ}

We're unsure if the website is profiting.

Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Link.springer.com could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {πŸ”}

pubmed, google, scholar, cas, central, liver, fibrosis, cell, zhang, aging, cells, senescence, mol, sci, liu, cellular, wang, article, hepatic, role, disease, diseases, cancer, med, int, res, oxidative, stress, biol, antioxidants, mitochondrial, inflammation, rev, mechanisms, reactive, oxygen, clin, ros, progression, species, han, dysfunction, treatment, molecular, chronic, signaling, gastroenterol, almalki, matrix, chen,

Topics {βœ’οΈ}

pluripotent-stem-cell-derived hepatic cells metal-organic framework-mediated synthesis salem salman almujri month download article/chapter ccl4-induced liver fibrosis reactive oxygen species-induced acetaminophen-mediated adverse interactions drives telomere-dependent disease regulating cgas-sting pathway atr/chk1 pathway modulation castruita-de la rosa orange-red keto carotenoid pnpla3-i148m variant promotes uv radiation-induced inflammation caspase-3/gsdme signalling pathway extracellular matrix-derived damage hutchinson-gilford progeria syndrome exploring ncrna-mediated regulation aged-related liver aging mitochondrial-mediated nuclear remodeling umm al-qura university ros-induced ros release references adjei-mosi anti-liver fibrosis effects reactive oxygen species hepatic stellate cells malat1-emt axis induce cell damage age-dependent loss privacy choices/manage cookies article biogerontology aims cellular senescence induction full article pdf nox4/nlrp3 inflammasome single-cell analysis cosmet laser ther accepted manuscript version cancer drug delivery senescent cell types morales-rosales sl alcoholic liver disease liver fibrosis/cirrhosis mediating astrocyte damage curcumin-based nanoformulations ramirez-acuΓ±a jm mitochondrial dysfunction disorders pham-huy additional information publisher' eliminating senescent cells chronic liver disease

Questions {❓}

  • Fallowfield J, Hayes P (2011) Pathogenesis and treatment of hepatic fibrosis: is cirrhosis reversible?
  • Khanam A, Saleeb PG, Kottilil S (2021) Pathophysiology and treatment options for hepatic fibrosis: can it be completely cured?
  • Ndhlala AR, Moyo M, Van Staden J (2010) Natural antioxidants: fascinating or mythical biomolecules?
  • Nousis L, Kanavaros P, Barbouti A (2023) Oxidative stress-induced cellular senescence: is labile iron the connecting link?
  • Ohtani N (2022) The roles and mechanisms of senescence-associated secretory phenotype (SASP): can it be controlled by senolysis?
  • Santoro A, Bientinesi E, Monti D (2021) Immunosenescence and inflammaging in the aging process: age-related diseases or longevity?

Schema {πŸ—ΊοΈ}

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         description:Ageing is an inevitable and multifaceted biological process that impacts a wide range of cellular and molecular mechanisms, leading to the development of various diseases, such as liver fibrosis. Liver fibrosis progresses to cirrhosis, which is an advanced form due to high amounts of extracellular matrix and restoration of normal liver structure with failure to repair damaged tissue and cells, marking the end of liver function and total liver failure, ultimately death. The most important factors are reactive oxygen species (ROS) and cellular senescence. Oxidative stress is defined as an impairment by ROS, which are by-products of the mitochondrial electron transport chain and other key molecular pathways that induce cell damage and can activate cellular senescence pathways. Cellular senescence is characterized by pro-inflammatory cytokines, growth factors, and proteases secreted by senescent cells, collectively known as the senescence-associated secretory phenotype (SASP). The presence of senescent cells, which disrupt tissue architecture and function and increase senescent cell production in liver tissues, contributes to fibrogenesis. Hepatic stellate cells (HSCs) are activated in response to chronic liver injury, oxidative stress, and senescence signals that drive excessive production and deposition of extracellular matrix. This review article aims to provide a comprehensive overview of the pathogenic role of ROS and cellular senescence in the aging liver and their contribution to fibrosis.
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      headline:Aging, ROS, and cellular senescence: a trilogy in the progression of liver fibrosis
      description:Ageing is an inevitable and multifaceted biological process that impacts a wide range of cellular and molecular mechanisms, leading to the development of various diseases, such as liver fibrosis. Liver fibrosis progresses to cirrhosis, which is an advanced form due to high amounts of extracellular matrix and restoration of normal liver structure with failure to repair damaged tissue and cells, marking the end of liver function and total liver failure, ultimately death. The most important factors are reactive oxygen species (ROS) and cellular senescence. Oxidative stress is defined as an impairment by ROS, which are by-products of the mitochondrial electron transport chain and other key molecular pathways that induce cell damage and can activate cellular senescence pathways. Cellular senescence is characterized by pro-inflammatory cytokines, growth factors, and proteases secreted by senescent cells, collectively known as the senescence-associated secretory phenotype (SASP). The presence of senescent cells, which disrupt tissue architecture and function and increase senescent cell production in liver tissues, contributes to fibrogenesis. Hepatic stellate cells (HSCs) are activated in response to chronic liver injury, oxidative stress, and senescence signals that drive excessive production and deposition of extracellular matrix. This review article aims to provide a comprehensive overview of the pathogenic role of ROS and cellular senescence in the aging liver and their contribution to fibrosis.
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         Cell Biology
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External Links {πŸ”—}(495)

Analytics and Tracking {πŸ“Š}

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