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LINK . SPRINGER . COM {}

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  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
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We are analyzing https://link.springer.com/article/10.1007/s10522-024-10175-x.

Title:
Aging through the lens of mitochondrial DNA mutations and inheritance paradoxes | Biogerontology
Description:
Mitochondrial DNA encodes essential components of the respiratory chain complexes, serving as the foundation of mitochondrial respiratory function. Mutations in mtDNA primarily impair energy metabolism, exerting far-reaching effects on cellular physiology, particularly in the context of aging. The intrinsic vulnerability of mtDNA is increasingly recognized as a key driver in the initiation of aging and the progression of its related diseases. In the field of aging research, it is critical to unravel the intricate mechanisms underpinning mtDNA mutations in living organisms and to elucidate the pathological consequences they trigger. Interestingly, certain effects, such as oxidative stress and apoptosis, may not universally accelerate aging as traditionally perceived. These phenomena demand deeper investigation and a more nuanced reinterpretation of current findings to address persistent scientific uncertainties. By synthesizing recent insights, this review seeks to clarify how pathogenic mtDNA mutations drive cellular senescence and systemic health deterioration, while also exploring the complex dynamics of mtDNA inheritance that may propagate these mutations. Such a comprehensive understanding could ultimately inform the development of innovative therapeutic strategies to counteract mitochondrial dysfunctions associated with aging.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
  • Business & Finance

Content Management System {📝}

What CMS is link.springer.com built with?


Link.springer.com uses PLONE.

Traffic Estimate {📈}

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.
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How Does Link.springer.com Make Money? {💸}

We find it hard to spot revenue streams.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Link.springer.com could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {🔍}

pubmed, article, google, scholar, cas, mitochondrial, central, dna, aging, cell, biol, mutations, sci, mol, mtdna, httpsdoiorgs, res, oxidative, stress, role, rev, diseases, mitochondria, nat, ageing, genet, front, apoptosis, genetic, damage, disease, metabolism, mechanisms, med, cancer, cells, human, wang, function, effects, cellular, metab, proc, dev, nucleic, acids, httpsdoiorg, liu, inheritance, energy,

Topics {✒️}

month download article/chapter transient cell-cycle arrest base-excision repair deficiency ultra-sensitive sequencing reveals stress-induced ribonucleoprotein granules de-fusing mitochondria defuses age-specific gene expression p53/p21-independent manner cx43/mir21 pathway leads mitochondrial-induced epigenetic modifications mitochondria-derived peptide mots runyu liang & yongyin huang martinez de toda full article pdf da silva asr late-onset mitochondrial disease patel mr severe germ-line bottleneck article biogerontology aims exercise-induced oxidative stress sex-specific cardiac function mitochondrial dna mutagenesis mitochondrial life cycle gustafsson cm mitochondrial nd4 gene dna polymerase γ contreras ga mitochondrial dna replication impair holoenzyme stability privacy choices/manage cookies mitochondrial dna damage affect mitochondrial functions article number 33 rattan sis mitochondrial genomic integrity mitochondrial dna mutations de la fuente thermogenic brown fats mitochondrial dna hypomorph dna damage responses mammalian mitochondrial dna article chen lee w mitochondrial genetic variation mitochondrial genetic drift developmental genetic bottleneck mitochondrial dysfunction plays central role somatic mitochondrial mutations ogg1 requires cohesin

Questions {❓}

  • Beekman M, Dowling DK, Aanen DK (2014) The costs of being male: are there sex-specific effects of uniparental mitochondrial inheritance?
  • Childs BG, Baker DJ, Kirkland JL et al (2014) Senescence and apoptosis: dueling or complementary cell fates?
  • Darcy J, Tseng Y-H (2019) ComBATing aging—does increased brown adipose tissue activity confer longevity?
  • Keaney TA, Wong HWS, Dowling DK et al (2020) Sibling rivalry versus mother’s curse: can kin competition facilitate a response to selection on Male mitochondria?
  • Lafforgue G, Lefebvre M, Michon T, Elena SF (2023) How do plant RNA viruses overcome the negative effect of Muller’s ratchet despite strong transmission bottlenecks?
  • Powers SK, Deminice R, Ozdemir M et al (2020) Exercise-induced oxidative stress: friend or foe?
  • Zhou RR, Wang B, Wang J et al (2010) Is the mitochondrial cloud the selection machinery for preferentially transmitting wild-type mtDNA between generations?

Schema {🗺️}

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         headline:Aging through the lens of mitochondrial DNA mutations and inheritance paradoxes
         description:Mitochondrial DNA encodes essential components of the respiratory chain complexes, serving as the foundation of mitochondrial respiratory function. Mutations in mtDNA primarily impair energy metabolism, exerting far-reaching effects on cellular physiology, particularly in the context of aging. The intrinsic vulnerability of mtDNA is increasingly recognized as a key driver in the initiation of aging and the progression of its related diseases. In the field of aging research, it is critical to unravel the intricate mechanisms underpinning mtDNA mutations in living organisms and to elucidate the pathological consequences they trigger. Interestingly, certain effects, such as oxidative stress and apoptosis, may not universally accelerate aging as traditionally perceived. These phenomena demand deeper investigation and a more nuanced reinterpretation of current findings to address persistent scientific uncertainties. By synthesizing recent insights, this review seeks to clarify how pathogenic mtDNA mutations drive cellular senescence and systemic health deterioration, while also exploring the complex dynamics of mtDNA inheritance that may propagate these mutations. Such a comprehensive understanding could ultimately inform the development of innovative therapeutic strategies to counteract mitochondrial dysfunctions associated with aging.
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            Genetic bottleneck
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            Cell Biology
            Geriatrics/Gerontology
            Developmental Biology
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      headline:Aging through the lens of mitochondrial DNA mutations and inheritance paradoxes
      description:Mitochondrial DNA encodes essential components of the respiratory chain complexes, serving as the foundation of mitochondrial respiratory function. Mutations in mtDNA primarily impair energy metabolism, exerting far-reaching effects on cellular physiology, particularly in the context of aging. The intrinsic vulnerability of mtDNA is increasingly recognized as a key driver in the initiation of aging and the progression of its related diseases. In the field of aging research, it is critical to unravel the intricate mechanisms underpinning mtDNA mutations in living organisms and to elucidate the pathological consequences they trigger. Interestingly, certain effects, such as oxidative stress and apoptosis, may not universally accelerate aging as traditionally perceived. These phenomena demand deeper investigation and a more nuanced reinterpretation of current findings to address persistent scientific uncertainties. By synthesizing recent insights, this review seeks to clarify how pathogenic mtDNA mutations drive cellular senescence and systemic health deterioration, while also exploring the complex dynamics of mtDNA inheritance that may propagate these mutations. Such a comprehensive understanding could ultimately inform the development of innovative therapeutic strategies to counteract mitochondrial dysfunctions associated with aging.
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         Evolutionary selection
         Genetic bottleneck
         Mother’s curse
         Cell Biology
         Geriatrics/Gerontology
         Developmental Biology
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