At a glance
What is it—and why does it matter?
An introduction is not yet available. The findings below address specific research questions, not a complete account of this peptide.
This published profile is a reference in progress. Findings retain their source context; missing topics are marked below.
What is it?
A molecule, not a product name.
This profile does not yet contain a published summary for this topic. This is a coverage gap, not evidence that no research exists.
How does it work?
Target, response, and disposition.
Mechanism
In this DNA damage–induced senescence setup, alterations in p21 homeostasis were used as evidence consistent with activation of the DNA damage response.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Although DNA damage response (DDR) was activated as seen by changes in p21 homeostasis, this did not always correlate with senescence levels, which indicates that DDR alone cannot account for all senescence characteristics.”
Impaired mitochondrial quality control and stress signalling machinery modulate senescence induction by genotoxic challenge. · Abstract
pubmed:42498093:a72f81b3713e:a72f81b3713e
What has been studied?
What the evidence says.
Study findings
In these mouse fibrosis models, the abstract reports cellular senescence features together with activation of the p53/p21 signaling pathway.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Here, we report that unilateral ureteral ligation (UUO) and folic acid (FA)-induced fibrotic mouse kidneys exhibited a marked senescent phenotype and activated p53/p21 pathway, accompanied by significant upregulation of ubiquitin-specific protease 11 (USP11).”
Ubiquitin-specific protease 11 promotes tubular cell senescence via inhibiting p53 ubiquitin degradation during renal fibrosis. · Abstract
pubmed:42448161:66d0459468db:66d0459468db
Study findings
Within this model, p21-homeostasis changes linked to DDR activation were not consistently aligned with measured senescence levels, suggesting p21/DDR markers and senescence readouts can diverge under some conditions.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Although DNA damage response (DDR) was activated as seen by changes in p21 homeostasis, this did not always correlate with senescence levels, which indicates that DDR alone cannot account for all senescence characteristics.”
Impaired mitochondrial quality control and stress signalling machinery modulate senescence induction by genotoxic challenge. · Abstract
pubmed:42498093:a72f81b3713e:a72f81b3713e
Study findings
In vitro exposure to recombinant granzyme K triggered senescence-associated signaling that includes the p53–p21–p16 axis in mouse lung epithelial and alveolar macrophage cell lines.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“In vitro, GZMK directly induced cellular senescence and activated the p53/p21/p16 pathway along with SASP factor expression.”
Targeting CD8+T cell-derived granzyme K alleviates radiation-induced pulmonary fibrosis by attenuating senescence and SASP. · RESULTS
pubmed:42409150:8b1b800fea5a:8b1b800fea5a
Study findings
In a DNA damage–induced senescence model using mouse embryonic fibroblasts, p21 abundance (total and nuclear) was used as a senescence-related readout alongside other markers.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Senescence was characterised using multiple complementary markers, including the proportion of high senescence-associated β-galactosidase-positive cells, nuclear size, total and nuclear p21 abundance, and transcriptional analysis of p16, p21 and genes associated with cell-cycle regulation and stress signalling.”
Impaired mitochondrial quality control and stress signalling machinery modulate senescence induction by genotoxic challenge. · Abstract
pubmed:42498093:a72f81b3713e:a72f81b3713e
Study findings
The study’s senescence profiling included transcriptional assessment of p21 (along with p16 and other stress/cell-cycle genes) in MEFs subjected to genotoxic stress.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Senescence was characterised using multiple complementary markers, including the proportion of high senescence-associated β-galactosidase-positive cells, nuclear size, total and nuclear p21 abundance, and transcriptional analysis of p16, p21 and genes associated with cell-cycle regulation and stress signalling.”
Impaired mitochondrial quality control and stress signalling machinery modulate senescence induction by genotoxic challenge. · Abstract
pubmed:42498093:a72f81b3713e:a72f81b3713e
Study findings
Recombinant granzyme K acted as a pro-senescent stimulus in cell culture, directly inducing cellular senescence.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“In vitro, GZMK directly induced cellular senescence and activated the p53/p21/p16 pathway along with SASP factor expression.”
Targeting CD8+T cell-derived granzyme K alleviates radiation-induced pulmonary fibrosis by attenuating senescence and SASP. · RESULTS
pubmed:42409150:8b1b800fea5a:8b1b800fea5a
Study findings
In a mouse ischemia-reperfusion injury context, tubule-specific Amd1 knockdown was associated with increased p21 (a p53-pathway cell-cycle checkpoint marker) versus wild-type controls.
1 cited source · Study independence not established
Animal or laboratory findings do not establish benefit or safety in people.
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Evidence boundary: Applies only to the source-defined population, formulation, dose, and assessment period.
Exact passages, locators, and provenance
- supports · Source-backed record
“Compared with wild-type controls,Amd1cKDmice exhibited aggravated tubular injury, an over two-fold increase in SA-β-gal-positive areas, elevated p21, and reduced Ki67+ proliferation.”
AMD1-mediated polyamine metabolism governs tubular repair fate by restraining senescence after kidney injury. · Abstract
pubmed:42289383:84508b74687b:84508b74687b
Risks and interactions
Risks, organized for scanning.
This profile does not yet contain a published summary for this topic. This is a coverage gap, not evidence that no research exists.
Products and regulatory status
Same ingredient. Different records.
This profile does not yet contain a published summary for this topic. This is a coverage gap, not evidence that no research exists.
Administration context
The practical clinical context.
This profile does not yet contain a published summary for this topic. This is a coverage gap, not evidence that no research exists.
Additional research & classification gaps
8 archived statements are kept separate from drug-effect findings. Media studies, economic models, methods, and records with unresolved scope are not used as medical-effect evidence.
Inspect contextual research (8)
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Intervening against granzyme K was associated with reduced fibrosis in the study’s context.
Research context only—not evidence of a treatment effect.
- Targeting CD8+T cell-derived granzyme K alleviates radiation-induced pulmonary fibrosis by attenuating senescence and SASP.
Targeting GZMK alleviated fibrosis, highlighting its potential as a therapeutic target for radiation-induced lung injury.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Blocking granzyme K activity in vivo was associated with lower senescent cell burden and reduced SASP inflammatory/pro-fibrotic mediators (IL-6, TNF-α, TGF-β).
Research context only—not evidence of a treatment effect.
- Targeting CD8+T cell-derived granzyme K alleviates radiation-induced pulmonary fibrosis by attenuating senescence and SASP.
In vivo inhibition of GZMK markedly attenuated lung collagen deposition, myofibroblast activation, senescent cell burden, and levels of SASP factors (IL-6, TNF-α, TGF-β).
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
In the fibrotic phase of radiation-induced lung injury, granzyme K expression rose and was chiefly attributed to infiltrating CD8+ T cells.
Research context only—not evidence of a treatment effect.
- Targeting CD8+T cell-derived granzyme K alleviates radiation-induced pulmonary fibrosis by attenuating senescence and SASP.
GZMK was significantly upregulated during the fibrotic phase and localized predominantly to infiltrating CD8+T cells.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Inhibiting granzyme K in vivo was associated with reduced fibrotic remodeling markers, including collagen deposition and myofibroblast activation.
Research context only—not evidence of a treatment effect.
- Targeting CD8+T cell-derived granzyme K alleviates radiation-induced pulmonary fibrosis by attenuating senescence and SASP.
In vivo inhibition of GZMK markedly attenuated lung collagen deposition, myofibroblast activation, senescent cell burden, and levels of SASP factors (IL-6, TNF-α, TGF-β).
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Granzyme K is characterized here as an inflammatory amplifier, implying it can enhance inflammatory signaling.
Research context only—not evidence of a treatment effect.
- Targeting CD8+T cell-derived granzyme K alleviates radiation-induced pulmonary fibrosis by attenuating senescence and SASP.
Granzyme K (GZMK) is an inflammatory amplifier, yet its role in promoting RIPF by regulating cellular senescence remains unknown.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
The background frames radiation-induced pulmonary fibrosis as being driven by cellular senescence and the senescence-associated secretory phenotype (SASP).
Research context only—not evidence of a treatment effect.
- Targeting CD8+T cell-derived granzyme K alleviates radiation-induced pulmonary fibrosis by attenuating senescence and SASP.
Cellular senescence and the senescence-associated secretory phenotype (SASP) are central drivers of this condition.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
Granzyme K is positioned as a mechanistic driver of radiation-induced pulmonary fibrosis through induction of cellular senescence and the senescence-associated secretory phenotype (SASP).
Research context only—not evidence of a treatment effect.
- Targeting CD8+T cell-derived granzyme K alleviates radiation-induced pulmonary fibrosis by attenuating senescence and SASP.
This study demonstrates that CD8+T cell-derived GZMK drives RIPF by promoting cellular senescence and SASP.
1 cited source · Study independence not established
How to read this evidence
Sources and study IDs describe provenance, not clinical strength. Several articles can report the same study; one study can support several distinct findings. No clinical strength rating has been assigned here.
1 cited passage across 1 source record. 1 publication group(s) lack a resolved study identity.
In this source, p53/p21 pathway activation is described as a key initiating event in renal tubular epithelial cell senescence.
Research context only—not evidence of a treatment effect.
- Ubiquitin-specific protease 11 promotes tubular cell senescence via inhibiting p53 ubiquitin degradation during renal fibrosis.
Emerging evidence has established that renal tubular epithelial cell (TEC) senescence is an essential driver of renal fibrosis, while the activation of p53/p21 pathway plays a key role in initiating TEC senescence.
Research status + gaps
What still needs better answers?
- No publishable claim yet for: administration, contraindication, interaction, regulatory, safety
- 81 compiled claim(s) withheld by automated assurance: assurance_score_below_0.58 (55), assurance_score_below_0.72 (24), current_regulatory_source_required (19), extraction_ambiguity (51), high_risk_requires_regulatory_or_two_independent_sources (26), no_direct_support (79)
- A source-backed introductory overview is not yet available.
These are the limits of this profile, not an exhaustive list of scientific uncertainties.
References + discovery
Open the records yourself.
- AMD1-mediated polyamine metabolism governs tubular repair fate by restraining senescence after kidney injury. ↗
pubmed · published 2026-12-01 · retrieved 2026-08-28T12:35:21Z
- Targeting CD8+T cell-derived granzyme K alleviates radiation-induced pulmonary fibrosis by attenuating senescence and SASP. ↗
pubmed · published 2026-10-01 · retrieved 2026-09-05T09:00:33Z
- Ubiquitin-specific protease 11 promotes tubular cell senescence via inhibiting p53 ubiquitin degradation during renal fibrosis. ↗
pubmed · published 2026-11-01 · retrieved 2026-09-05T09:00:33Z
- Impaired mitochondrial quality control and stress signalling machinery modulate senescence induction by genotoxic challenge. ↗
pubmed · published 2026-11-01 · retrieved 2026-09-05T09:00:33Z
Publication history and provenance
Version 2 · Automated assessment · 2026-09-05T09:00:33Z
94f3d9924fe5bab8c4078270bdfda2401bd8583bc9c353ef5f953835c8b699b7