Developmental Morphogens and Adult Liver Repair

Machado, Mariana Verdelho; Diehl, Anna Mae

doi:10.1002/9781119436812.ch43

Cited by 1 publication

(1 citation statement)

References 153 publications

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“…Moreover, somatic construction and developmental transformation of the soma cannot continue indefinitely because physical limitations, morphogenetic construction rules, phyletic developmental constraints, laws of diffusion, hydraulics, and physical support prevent it [ 55 ]. Finally, once development is complete, signaling pathways for mechanisms regulating novel pattern formation are typically inactivated, thereby preventing further developmental change in structures related to morphogenesis [ 65 ].…”

Section: Redundant Expression Of the Last Morphogenetic Stagementioning

confidence: 99%

A Mechanistic Theory of Development-Aging Continuity in Humans and Other Mammals

Walker¹

2022

Cells

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There is consensus among biogerontologists that aging occurs either as the result of a purposeful genome-based, evolved program or due to spontaneous, randomly occurring, maladaptive events. Neither concept has yet identified a specific mechanism to explain aging’s emergence and acceleration during mid-life and beyond. Presented herein is a novel, unifying mechanism with empirical evidence that describes how aging becomes continuous with development. It assumes that aging emerges from deterioration of a regulatory process that directs morphogenesis and morphostasis. The regulatory system consists of a genome-wide “backbone” within which its specific genes are differentially expressed by the local epigenetic landscapes of cells and tissues within which they reside, thereby explaining its holistic nature. Morphostasis evolved in humans to ensure the nurturing of dependent offspring during the first decade of young adulthood when peak parental vitality prevails in the absence of aging. The strict redundancy of each morphostasis regulatory cycle requires sensitive dependence upon initial conditions to avoid initiating deterministic chaos behavior. However, when natural selection declines as midlife approaches, persistent, progressive, and specific DNA damage and misrepair changes the initial conditions of the regulatory process, thereby compromising morphostasis regulatory redundancy, instigating chaos, initiating senescence, and accelerating aging thereafter.

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Section: Redundant Expression Of the Last Morphogenetic Stagementioning

confidence: 99%

A Mechanistic Theory of Development-Aging Continuity in Humans and Other Mammals

Walker¹

2022

Cells

View full text Add to dashboard Cite

show abstract

Developmental Morphogens and Adult Liver Repair

Cited by 1 publication

References 153 publications

A Mechanistic Theory of Development-Aging Continuity in Humans and Other Mammals

A Mechanistic Theory of Development-Aging Continuity in Humans and Other Mammals

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