Cell Programmed Death

Necroptosis: A Key Target in Cancer & Beyond Therapeutics

Necroptosis is a form of programmed cell death with characteristics of both necrosis and apoptosis, triggered by death receptors (e.

Disulfidptosis: A Promising Target For Cancer Management

Disulfidptosis is a newly identified form of programmed cell death (PCD) defined by actin cytoskeleton collapse triggered by disulfide stress.

Cuproptosis: An Emerging Target In Cancer Therapy

Cuproptosis represents a distinctive regulated cell death mode elicited by mitochondrial copper.

Cell Death & Disease

Cell death is essential for development, growth, and survival, aiding tissue remodeling and homeostasis by removing unwanted or harmful cells.

Ferroptosis: A Key Regulator in Cancer Therapy and Beyond

Ferroptosis, a form of regulated cell death characterized by iron dependence and lipid peroxidation, has emerged as a critical player in various physiological and pathological processes.

The Core Of Inflammatory Stress: The Apoptosome, Inflammasome, And PIDDosome

The apoptosome, inflammasome, and PIDDosome are supramolecular caspase-activation platforms that translate cellular stress into apoptosis, inflammation, cell-cycle control, or differentiation.

Entosis: A Cell-in-Cell Death Process

Entosis is a nonphagocytic cell-in-cell process in which one living cell actively enters another and may subsequently die inside the host cell.

Metabolic Homeostasis Determines the Plasticity of Regulated Cell Death

Metabolic homeostasis is the regulated balance of nutrients, energy, reducing power, ions, and macromolecular turnover that allows cells to adapt without crossing a lethal threshold.

Evolution and Cutting-Edge Innovations in Cell-Death Detection Methods

Cell-death detection has evolved from static morphology to multiparameter, mechanism-aware measurement.

Erebosis: A Newly Described Cell-Death Phenomenon

Erebosis describes a cell-death-like state discovered during homeostatic replacement of enterocytes in the adult Drosophila intestine.

Inflammasome Pathways Overview

Inflammasomes are cytosolic multiprotein platforms that convert microbial or cellular danger detection into inflammatory caspase activation, IL-1β and IL-18 maturation, and often gasdermin-dependent pyroptosis.

Regulated Cell Death (RCD) in Cardiomyocytes

Regulated cell death in cardiomyocytes comprises molecular programs that eliminate irreversibly damaged heart muscle cells and can, in principle, be modulated.

Therapeutic Targeting of Non-Apoptotic Cell Death

Non-apoptotic regulated cell death comprises mechanistically defined programs that kill cells without relying primarily on canonical apoptotic execution.

Triaptosis: A Unique Cell Death Pathway

Triaptosis is an emerging oxidative, endosome-dependent cell-death modality defined from a 2024 study of menadione sodium bisulfite, a water-soluble vitamin K precursor.

Apoptosis Resistance in Metastatic Cancer

Apoptosis resistance is the capacity of malignant cells to avoid caspase-dependent death despite oncogenic stress, therapy, immune attack, or loss of tissue attachment.

Pyroptosis, PANoptosis, and Immunity

Pyroptosis is a lytic inflammatory death program executed by gasdermin pores, whereas PANoptosis describes coordinated inflammatory death with pyroptotic, apoptotic, and necroptotic components that cannot be explained by any one pathway alone.

Epigenetics and Cell Death in Cancer Therapy

Epigenetics regulates gene activity without changing DNA sequence through DNA methylation, histone modification, chromatin remodeling, non-coding RNAs, and RNA modifications.

Crosstalk and Interconnection Between Cell Death Pathways

Regulated cell-death pathways were initially organized as separate modules defined by characteristic morphology and core effectors.

Phagoptosis: Cell Death via Phagocytosis

Phagoptosis is death caused by engulfment of a cell that was viable when phagocytosis began.

Methuosis: Macropinocytotic Cell Death Overcoming Tumor Drug Resistance

Methuosis is a non-apoptotic cell-death phenotype marked by extreme accumulation of macropinosome- and endosome-derived vacuoles, progressive cytoplasmic disruption, and loss of plasma-membrane integrity.

Anoikis: A Barrier Inhibiting Distant Metastasis of Cancer Cells

Anoikis is an apoptotic program triggered when anchorage-dependent cells lose appropriate contact with the extracellular matrix.

RCDs in Tumor Metabolism and Tumor Immunity

Metabolic context determines death susceptibility.

NECSO: A Novel Necrotic Cell Death Characterized by Sodium Overload

Ion overload serves as an execution mechanism.

Mitoxyperilysis: A Novel Cell Death Induced by Metabolic Dysregulation

Mitoxyperilysis is a mitochondria-driven form of lytic cell death reported in 2025 after experiments designed to reproduce the coexistence of innate immune activation and metabolic disruption.

Tumor Drug Resistance and Cuproptosis Regulation

Cuproptosis is a copper-dependent regulated cell-death mechanism caused by copper binding to lipoylated proteins of the mitochondrial tricarboxylic-acid cycle, promoting protein aggregation, loss of iron-sulfur-cluster proteins, and proteotoxic stress.

BCMA-Targeted CAR-T for MM

B-cell maturation antigen is a highly relevant surface target on malignant plasma cells, making BCMA-directed CAR-T therapy a major advance for relapsed or refractory multiple myeloma.

Immune-activating effects of oncolytic virus therapy

Oncolytic viruses are designed or selected to infect and replicate preferentially in malignant tissue, causing tumor lysis while stimulating immunity.

Tumor-Infiltrating Lymphocyte (TIL) Therapy

Tumor-infiltrating lymphocyte therapy expands a patient’s own lymphocytes from a resected tumor and returns them after lymphodepleting conditioning.

Advancing the Application of Immunotherapy Targeting MAPK/ERK Signaling

The RAS–RAF–MEK–ERK pathway drives proliferation, survival, differentiation, and adaptation in many cancers.

Tumor-Busting: Cancer-Mimicking Peptide Immunotherapy

Cancer-mimicking peptide immunotherapy uses altered peptides, mimotopes, or selected peptide ligands to provoke immunity that cross-recognizes a tumor antigen.

T-cell immunotherapy and cancer treatment

T-cell immunotherapy encompasses treatments that release endogenous T cells from inhibition, redirect them with antibodies, expand tumor-reactive populations, or engineer new antigen receptors.

Bispecific antibodies and cancer treatment

Bispecific antibodies bind two different epitopes or antigens within one therapeutic molecule.

Neoadjuvant immunotherapy and cancer treatment

Neoadjuvant immunotherapy treats a resectable cancer before surgery, when the primary tumor and its draining lymphatic network remain available as sources of antigen and immune priming.

Immune synapses: molecular mechanisms and therapeutic significance

The immunological synapse is the organized contact through which a T cell communicates with an antigen-presenting cell or a cytotoxic lymphocyte attacks a target.

Adoptive Cell Therapy (ACT) and Cancer Treatment

Adoptive cell therapy transfers immune cells with selected or engineered antitumor activity into a patient.

Advances in Breast Cancer Immunotherapy

Breast cancer was historically considered less immunogenic than melanoma or lung cancer, but that view changed as molecular subtypes, tumor-infiltrating lymphocytes, and checkpoint responses were studied separately.

CAR-T Therapy Challenges: Tumor Relapse

Tumor relapse is the principal limit on the curative potential of CAR-T therapy.

CAR-T and Gynecologic Cancers

Gynecologic cancers are attractive candidates for CAR-T therapy because recurrent ovarian, cervical, and endometrial tumors often have limited curative options and can express accessible surface antigens.

Radiation and Tumor Immune Microenvironment

Radiotherapy is no longer viewed only as a local method for damaging tumor DNA.

CAR-T Therapy for Lymphoma

Chimeric antigen receptor T-cell therapy has changed the treatment framework for relapsed or refractory B-cell lymphoma by converting a patient’s T cells into living drugs.

Regulation of Cardiovascular Pathology by Copper Homeostasis and Cuproptosis

Copper is an essential redox-active trace element required for cytochrome oxidase, antioxidant enzymes, connective-tissue crosslinking, and other cardiovascular functions.

Mitochondrial homeostasis and myocardial health

Mitochondrial homeostasis is the coordinated maintenance of organelle protein quality, genome expression, membrane potential, dynamics, calcium signaling, biogenesis, and removal.

Oxidative-inflammatory axis in organ ischemia-reperfusion injury

Ischemia-reperfusion injury is the paradoxical tissue damage that develops when blood flow returns after oxygen and nutrient deprivation.

SIRT3 and Cardiovascular Diseases

Sirtuin 3 (SIRT3) is a mitochondrial NAD+-dependent deacetylase that adjusts enzyme activity through lysine deacetylation.

Ferroptosis and Cardiovascular Disease

Ferroptosis is an iron-dependent form of regulated cell death driven by lethal accumulation of phospholipid hydroperoxides.

PANoptosis and Cardiovascular Diseases

PANoptosis is an inflammatory lytic cell-death program in which pyroptotic, apoptotic, and necroptotic machinery is coordinated within a PANoptosome.

Cancer Stemness: Hallmarks And Plasticity

Cancer stemness describes a tumor-cell state marked by self-renewal, tumor initiation, differentiation capacity, therapeutic resistance, and plastic transitions between stem-like and non-stem-like phenotypes.

Cellular Senescence In Aging And Cancer

Cellular senescence in aging and cancer describes a stable cell-cycle arrest triggered by stress, damage, oncogene activation, or therapy.

Mechanisms Of Cancer Dormancy-Mediated Metastasis And Targeted Therapies

Cancer dormancy-mediated metastasis describes how disseminated tumor cells persist in distant tissues in a viable but non-proliferative state, evade therapy, and later reawaken to generate metastatic relapse.

Lipid Raft Remodeling Strategies For Inducing Tumor Cell Death

Lipid raft remodeling strategies for inducing tumor cell death target cholesterol- and sphingolipid-rich membrane microdomains that compartmentalize signaling proteins.