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Cellular senescence
Research brief

Review maps senescence regulatory network and proposed theranostic tools

This review maps the molecular network of cellular senescence across p53/p21, p16/RB, mitochondrial stress, cGAS-STING and mTOR-driven SASP programs, traces its rewiring in cancer, metabolic, skeletal and organ-specific degenerative diseases, and describes proposed theranostic approaches; clinical translation remains limited. [1]

Automatic summary · not editorially reviewed

The key findings

  1. The review maps senescence regulation through p53/p21, p16/RB, mitochondrial stress, cGAS-STING and mTOR-driven SASP programs. [1]

  2. The review traces how these mechanisms are rewired in cancer, metabolic and skeletal disorders, and organ-specific degenerative diseases. [1]

  3. Clinical translation of senescence theranostics remains limited by cell heterogeneity, off-target toxicity and missing standardized biomarkers. [1]

The source at a glance

Study type / format
Narrative review (abstract only)
Population / context
Cellular senescence mechanisms across cancer, metabolic, skeletal and organ-specific degenerative disease contexts
Summary based on
Study abstract
Original publication
September 15, 2026

Senescence network axes and SASP programs

The review describes cellular senescence as controlled by a complex, multidimensional regulatory network whose outputs shift with disease stage and tissue context. It maps the p53/p21 and p16/RB axes, mitochondrial stress pathways, and the cGAS-STING and mTOR-driven SASP programs. SASP here refers to the senescence-associated secretory program named in the source.

Supporting source [1]

Rewiring across cancer and degenerative diseases

The review traces how these mechanisms are rewired across a spectrum of pathological contexts, including cancer, metabolic and skeletal disorders, and organ-specific degenerative diseases. These are described as contexts in which the network's functional outputs change, not as proven causal roles.

Supporting source [1]

Proposed theranostic tools and translation limits

The review highlights theranostic innovations that integrate detection with intervention: enzyme-activatable prodrugs and probes exploiting markers such as SA-β-gal for simultaneous imaging and cell clearance, smart nanocarriers for spatiotemporally controlled delivery, and engineered immune cells to restore immunosurveillance against senescent cells. It also discusses emerging platforms for dynamic quantification of senescent burden in vivo, including molecular imaging probes and liquid biopsy signatures. Despite promising preclinical progress, clinical translation remains limited by senescent-cell heterogeneity, off-target toxicity and the lack of standardized biomarkers. The review offers a framework for precision strategies, not a validated product.

Supporting source [1]

How to interpret this

Abstract only; the full text was not reviewed. This is a review, so no primary study design, sample or follow-up is reported. The theranostic tools and the proposed framework are described as preclinical and not validated for clinical use.

Based on the study abstract; the full paper, tables and supplementary data were not reviewed.

Source & supporting passages

[1]
Multidimensional Regulatory Network of Cellular Senescence: From Mechanisms to Theranostics.

Lv Z, Liu Y, Liu Y, Tan Y, Man Y, Du S, Zhang Z, Lee LP, Chen QW, Liu Z. · europepmc.org · September 15, 2026

Read the quoted passagesIn the language of the original source
  1. Finding 1 ↑

    the p53/p21 and p16/RB axes
  2. Finding 2 ↑

    rewired across a spectrum of pathological contexts
  3. Finding 3 ↑

    clinical translation remains limited by senescent-cell heterogeneity

AI-assisted summary with linked source passages. No independent editorial or clinical review.

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