Apoptosis

Overview

Apoptosis is a tightly regulated form of programmed cell Death by which cells dismantle themselves through a defined molecular cascade, in contrast to the disordered membrane rupture of necrosis. It is characterized by chromatin condensation, nuclear fragmentation, cell shrinkage, and the formation of apoptotic bodies that are cleared by phagocytes without inflammation. Two principal pathways converge on effector caspases: the intrinsic, mitochondrial pathway governed by the BCL-2 protein family—including pro-apoptotic BAK and anti-apoptotic BCL-2—which controls cytochrome c release, and the extrinsic pathway initiated by Death-receptor ligation. Apoptosis is essential for embryonic development, immune homeostasis, and elimination of damaged or potentially malignant cells; its dysregulation contributes to cancer, neurodegeneration, and tissue injury. Triggers include oxidative stress, genotoxic and metabolic insults, and pharmacologic agents, and resistance to apoptosis is a recognized mechanism of treatment failure in tumor cells. Research relevant to this area examines apoptosis in stored platelets, acquired resistance to butyrate-induced apoptosis in colorectal cancer, oxidative stress and apoptosis in testicular tissue, the roles of BCL-2 and BAK in renal disease, prostate apoptosis response protein in metastasis, and nanoparticle-induced apoptotic activity in cancer cell lines. This peer-reviewed literature reflects the mechanistic and disease-related dimensions of programmed cell Death.

Research published in this journal

12 peer-reviewed articles, ranked by relevance. Each links to its DOI.

How this research is being cited

The 12 articles above have been cited 85 times in the scholarly literature. Citation data via OpenAlex and Crossref, updated Jun 2026.

• High-Intensity Interval and Aerobic Training Alleviate Cardiac Pathology, Apoptosis, and Atrial Fibrillation in Rats with Chronic Kidney Disease: The Roles of FGF23 and Klotho
  2026 · Biomolecules
• Zn glycine attenuates LPS-induced inflammatory bone loss in geese through suppression of osteoclastogenesis via reducing TLR-4/NFκB signaling
  2026 · Ecotoxicology and Environmental Safety
• Nephroprotective Effect of L-Carvone on a Mouse Model of LPS-Induced Sepsis-Associated Renal Injury via Regulation of TLR4/NF-κB/AP-1/IRF-3 and Nrf2/iNOS Molecular Signaling Cascades
  2026 · Journal of Taibah University Medical Sciences
• L-carvone alleviates lipopolysaccharide-Induced acute kidney injury via modulating MyD88-dependent and independent signaling pathways in Mice
  2026 · Molecular Biology Reports
• Fraisinib in a Shell: Liposomal Encapsulation of a GARS1 Inhibitor for Controlled Anticancer Delivery
  2026 · AAPS PharmSciTech
• Monosodium glutamate exacerbated the lipopolysaccharide-induced reproductive toxicity of male Wistar rats
  2025 · BMC Pharmacology and Toxicology
• Atrazine alters nitric oxide secretion and cytokines production in LPS-stimulated BalB/c mice, RAW264.7 macrophage and THP-1 cell lines
  2025 · Chemosphere
• Meprin β regulates osteopontin-signaling in ischemia/reperfusion-induced kidney injury
  2025 · BMC Nephrology

A sample of recent works citing this journal's research on Apoptosis, linking to each citing work.

This page summarises published research for orientation; it is not medical or professional advice.

Related topics