Apoptosis

Overview

Apoptosis, or programmed cell death, is an evolutionarily conserved, energy-dependent mechanism by which cells dismantle themselves in an orderly, non-inflammatory manner to maintain tissue homeostasis and eliminate damaged or dangerous cells. It is controlled through the intrinsic mitochondrial pathway, regulated by the pro- and anti-apoptotic BCL-2 protein family including BAX, BAK, and BCL-2, and the extrinsic death-receptor pathway, with both routes activating initiator and effector caspases that cleave cellular substrates and produce DNA fragmentation, chromatin condensation, and apoptotic-body formation. In cancer genetics, evasion of apoptosis is a recognised hallmark of malignancy: loss of pro-apoptotic function, overexpression of survival proteins, and acquired resistance to apoptosis-inducing signals permit tumour growth, metastasis, and treatment failure. Conversely, many anticancer and experimental agents act by restoring or triggering apoptotic death, making apoptotic indices and regulatory-gene expression valuable readouts of therapeutic efficacy. Peer-reviewed research published in this area investigates resistance to butyrate-induced apoptosis in colorectal cancer cells, the role of BCL-2 and BAK genes, apoptosis in stored platelets, prostate apoptosis response protein-4 and metastasis suppression, oxidative-stress-induced apoptosis, and the apoptotic activity of nanoparticles and natural compounds, grounding the topic in the journal's focus on cancer-related cell death and biomarkers.

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 87 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
• Disruption of LINC00265/miR-101-3p axis using siRNA suppresses growth and promotes apoptosis in laryngeal cancer cells
  2026 · Gene Reports
• 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

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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