Review: tissue repair and regeneration decline across the human lifespan
This review maps how tissue repair shifts from scarless embryonic regeneration to fibrotic scarring in senescence, framing the decline as a systems-level reprogramming rather than pure degeneration. [1]
Automatic summary · not editorially reviewed
The key findings
The review maps a transition from scarless embryonic regeneration to fibrotic scarring and organ failure in senescence. [1]
The authors frame the decline as systems-level reprogramming with evolutionary trade-offs, not pure degeneration. [1]
The review contrasts severe regenerative restrictions in the adult central nervous system and myocardium with the liver's persistent but exhaustible resilience. [1]
The source at a glance
- Study type / format
- Review (abstract only)
- Population / context
- Human lifespan, from embryonic development to senescence
- Summary based on
- Study abstract
- Original publication
- August 24, 2026
Ontogenetic framework from embryo to senescence
The review proposes a framework mapping a continuous biological transition: from the scarless regenerative plasticity of embryonic development to irreversible fibrotic scarring and organ failure in senescence. It describes the capacity for tissue repair and regeneration as declining progressively across the human lifespan and calls this a fundamental driver of aging and chronic disease. The authors stress that this decline should not be read as a purely degenerative trajectory, but as a dynamic systems-level reprogramming in which evolutionary trade-offs favour tumour suppression, immune surveillance and reproductive fitness over long-term regenerative fidelity.
Supporting source [1]
Molecular drivers and organ-specific repair limits
At molecular and cellular level, the review links accumulating genomic instability, unresolvable DNA damage and mitochondrial dysfunction to a gradual overwhelming of intracellular quality-control mechanisms. It adds that epigenetic drift and chronic low-grade systemic inflammation (called "inflammaging") dismantle the stem cell niche, driving adult stem cell exhaustion and shifting wound healing from functional tissue replacement toward maladaptive fibrosis. It also contrasts organ-specific trajectories: severe regenerative restrictions in the adult central nervous system and myocardium versus the persistent but exhaustible resilience of the liver.
Supporting source [1]
Proposed clinical shift toward restoring tissue integrity
The review evaluates a proposed clinical paradigm shift: from passive management of age-related degeneration to active restoration of tissue integrity. It describes integrating systemic geroscience, which addresses global hallmarks of aging, with targeted bioengineering and in vivo epigenetic modulation, with regenerative medicine seeking to recreate permissive, youthful microenvironments. The authors state that mastering these ontogenetic principles holds potential to reactivate endogenous repair pathways, mitigate multi-organ collapse and extend human functional healthspan. These are stated aims and potential, not demonstrated outcomes.
Supporting source [1]
How to interpret this
This is an abstract of a review; the full text was not reviewed. The abstract reports no study design details, sample, follow-up or measured outcomes, and the proposed clinical approaches are described as potential, not demonstrated benefits.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Barrera-Saldaña HA, Fernández-Garza LE, Guillen-Silva F, Fajardo-Ramirez OR, Iñigo Pavlovich RF, Gómez-Gallardo FV, Rodriguez-Fuentes DE, Avila-Villalobos AY, Barrera-Barrera SA, Somoza RA. · europepmc.org · August 24, 2026