ReviewCell death and differentiation2017
Killers creating new life: caspases drive apoptosis-induced proliferation in tissue repair and disease.
Review in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
130 citing papers in PubMed, 238 citations in OpenAlex.
- Correlation of Long Non-Coding RNAs and Gene Expression in Response to Reverse Development of Turritopsis dohrnii.Marine biotechnology (New York, N.Y.) · 2026Article
- Microbiota-Derived Corisin Is Elevated in Early Cervical Neoplasia and Drives Pathogenic Cellular Programs.Cells · 2026Article
- The signaling and regulatory functions of dying cells and cell corpses.Communications biology · 2026Review
- Natural tissue immortality: Indefinite survival of sea cucumber explants.Science advances · 2026Article
- Article
- The paradigm-shifting roles of caspase-3 in cancer: from death towards resuscitation.Cancer cell international · 2026Review
- Single-cell RNA analysis reveals unexpected hemocyte plasticity and immune cell specialization in abioRxiv : the preprint server for biology · 2026Article
- Calcium signaling regulates apoptosis-induced proliferation in Drosophila.PLoS biology · 2026Article
- Apoptosis-resistant cells drive compensatory proliferation via cell-autonomous and non-autonomous functions of the initiator caspase Dronc.Nature communications · 2025Article
- EyaHOST, a modular genetic system for investigation of intercellular and tumor-host interactions in Drosophila melanogaster.Cell reports methods · 2025Article
- Cell Death, Compensatory Proliferation, and Cell Competition.Annual review of genetics · 2025Review
- A threshold level of JNK activates damage-responsive enhancers via JAK/STAT to promote tissue regeneration.Development (Cambridge, England) · 2025Article
- Programmed cell revival from imminent cell death enhances tissue repair and regeneration.The EMBO journal · 2025Article
- A new era in cancer therapy: targeting the Proteasome-Bcl-2 axis.Journal of experimental & clinical cancer research : CR · 2025Review
- Decoding the divide: what distinguishes apoptosis-induced proliferation from compensatory proliferation?Cell communication and signaling : CCS · 2025Review
- Article
- Remote ischemia precondition protects against renal IRI through apoptosis associated vesicles carrying MIF protein via modulating DUSP6/JNK signaling axis.Journal of nanobiotechnology · 2025Article
- Nucleic acid nanobiosystems for cancer theranostics: an overview of emerging trends and challenges.Nanomedicine (London, England) · 2025Review
- Article
- Activation of the Drosophila innate immune system accelerates growth in cooperation with oncogenic Ras.PLoS biology · 2025Article
70 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Apoptosis is a carefully orchestrated and tightly controlled form of cell death, conserved across metazoans. As the executioners of apoptotic cell death, cysteine-dependent aspartate-directed proteases (caspases) are critical drivers of this cellular disassembly. Early studies of genetically programmed cell death demonstrated that the selective activation of caspases induces apoptosis and the precise elimination of excess cells, thereby sculpting structures and refining tissues. However, over the past decade there has been a fundamental shift in our understanding of the roles of caspases during cell death-a shift precipitated by the revelation that apoptotic cells actively engage with their surrounding environment throughout the death process, and caspases can trigger a myriad of signals, some of which drive concurrent cell proliferation regenerating damaged structures and building up lost tissues. This caspase-driven compensatory proliferation is referred to as apoptosis-induced proliferation (AiP). Diverse mechanisms of AiP have been found across species, ranging from planaria to mammals. In this review, we summarize the current knowledge of AiP and we highlight recent advances in the field including the involvement of reactive oxygen species and macrophage-like immune cells in one form of AiP, novel regulatory mechanisms affecting caspases during AiP, and emerging clinical data demonstrating the critical importance of AiP in cancer.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.