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Necrosis

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...

Overview of Cell Death

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...

The Extrinsic Apoptotic Pathway

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...

Apoptosis

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...

The Intrinsic Apoptotic Pathway

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...

Cellular Injury IV: Necrosis

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...

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Related Experiment Video

Updated: Apr 21, 2026

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

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Programmed necrosis and necroptosis signalling.

Maria Feoktistova¹, Martin Leverkus

¹Section of Molecular Dermatology, Department of Dermatology, Venereology and Allergology, Medical Faculty Mannheim, University Heidelberg, Germany.

The FEBS Journal

|October 21, 2014

Summary

Necroptosis, a regulated form of necrosis, involves key proteins like RIPK1. This review explores the intracellular signaling pathways central to this cell death process.

Keywords:

cellular FLICE-inhibitory protein (cFLIP) isoforms necroptosis receptor-interacting serine/threonine protein kinase 1 receptor-interacting serine/threonine protein kinase 3 ripoptosome

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Area of Science:

Molecular Biology
Cell Biology
Biochemistry

Background:

The understanding of cell death has evolved beyond apoptosis to include regulated forms of necrosis.
Receptor-interacting serine/threonine protein kinase 1 (RIPK1), RIPK3, and mixed-lineage kinase domain-like protein are central to regulated necrosis.
RIPK1's dual role as a kinase and scaffold molecule is critical in cell death complexes.

Purpose of the Study:

To introduce the field of necroptosis.
To focus on the intracellular signaling pathways governing necroptosis.
To highlight the significance of RIPK1 in necroptosis regulation.

Main Methods:

Literature review of recent studies on necroptosis.
Analysis of molecular signaling platforms involved in cell death.
Focus on the role of RIPK1, RIPK3, and MLKL.

Main Results:

Necroptosis is a key regulated cell death pathway.
RIPK1, RIPK3, and MLKL form critical signaling platforms.
RIPK1's kinase and scaffold functions are crucial for necroptosis.

Conclusions:

Necroptosis is an emerging and dynamic area of cell death research.
Intracellular signaling pathways are key to understanding necroptosis.
Further research into RIPK1's role is vital for the field.