Apoptosis

Overview

Apoptosis is a tightly regulated form of programmed cell death by which an organism eliminates defective, damaged, superfluous, or potentially dangerous cells without provoking inflammation. It is essential to embryonic development, tissue remodelling, immune selection, and homeostasis, and its dysregulation underlies cancer, degenerative disease, and tissue injury. Execution proceeds through two convergent routes: the extrinsic pathway, triggered by death-receptor ligation, and the intrinsic mitochondrial pathway, governed by the balance of pro- and anti-apoptotic BCL-2 family proteins such as BCL-2 and BAK, which control mitochondrial outer-membrane permeabilization and downstream caspase activation. Oxidative stress is a recurrent upstream trigger, as seen when lipopolysaccharide promotes apoptosis in susceptible tissues. In oncology, resistance to apoptosis is a hallmark of malignancy: tumour cells acquire resistance to apoptotic stimuli such as butyrate, while restoring pro-apoptotic effectors like prostate apoptosis response protein-4 can suppress metastasis through mechanisms including upregulation of E-cadherin. Conversely, engineered agents and nanomaterials are exploited to induce apoptotic and cytotoxic responses in cancer cell lines, and platelet viability during storage reflects apoptotic processes relevant to transfusion medicine. The journal publishes peer-reviewed research on apoptotic signalling, its role in disease pathogenesis and therapeutic resistance, and its manipulation in cancer biology, haematology, and regenerative contexts.

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 89 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.

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