Transcript

Necrosis and apoptosis

From Osmosis from Elsevier · Episode page · Watch on YouTube

· 17 min · 2,055 words · 21 timestamped sections

This is the full, timestamped transcript of "Necrosis and apoptosis", an episode of Osmosis from Elsevier published December 23, 2025 (17 min, about 2,055 words). It mentions 11 people, works and ideas, including necrosis, apoptosis, capsase, coagulative necrosis, fat necrosis.

What is discussed, and when

  1. – 3:00: apoptosis, necrosis
  2. – 6:00: apoptosis, necrosis, tumor necrosis factor alpha, tumor necrosis factor receptor 1
  3. – 9:00: necrosis, apoptosis, coagulative necrosis, tumor necrosis factor receptor 1
  4. – 12:00: necrosis, coagulative necrosis
  5. – 15:00: necrosis, apoptosis, fat necrosis
  6. – 16:36: necrosis, fat necrosis

Notable quotes from "Necrosis and apoptosis"

  • To die. One way is by apoptosis, which is a form of programmed cell death. The second way is by necrosis, which is when cells die due to injury or disease.
    about necrosis · at
  • That binds to very appropriately named death receptors on the target cell membrane. One example being tumor necrosis factor receptor 1. The systolic end of this receptor dives…
    about tumor necrosis factor receptor 1 · at
  • First, there's coagulative necrosis, which occurs when a tissue becomes hypoxic, has low levels of oxygen, most commonly due to eskeeia. Hypoxia causes structural proteins to bend out of.
    about coagulative necrosis · at
  • Next, there's fat necrosis, which most commonly occurs when there's trauma to fatty organs that have a lot of atapost cells like the pancreas or the breasts.
    about fat necrosis · at

Who and what is mentioned in this episode?

Concepts & topics

Full transcript with timestamps

Generally speaking, cells have two ways to die. One way is by apoptosis, which is a form of programmed cell death. The second way is by necrosis, which is when cells die due to injury or disease. Overall, apoptosis occurs much more often than necrosis. One example is when our old skin cells undergo apoptosis and get replaced by new skin cells. Another example is in our hands and feet during fetal development. Initially, human hands and feet look like duck's feet with webs of skin connecting the fingers, but the cells in the webbing undergo apoptosis, and that allows us to form individual digits that allow us to pick our nose and play the piano.

In contrast, necrosis occurs less frequently. An example of necrosis is when a blood vessel that feeds an area of the body, say the big toe, becomes blocked and can't deliver oxygen and nutrients to the cells like usual. It causes eskeeia and the cells die. As a result, the tissues of the toe will turn a nasty shade of black, signaling necrosis. Enjoying our osmosis videos? Unlock your full potential with an Osmosis subscription. Get unlimited access to every Osmosis feature and resource with a free 7-day trial. In apoptosis, there are two activating mechanisms. The intrinsic pathway, also called the mitochondrial pathway, and the exttrinsic pathway, also called the death receptor pathway.

The intrinsic pathway occurs when a cell is exposed to stress like radiation, hypoxia or low oxygen, a high intracellular concentration of calcium ions or oxidative stress which is where reactive molecules with unpaired electrons called free radicals steal electrons from nearby molecules. These stressors cause two intracellular proteins backs and back to move the cytool to the mitochondria. Once in the mitochondria, backs and back pierce the outer mitochondrial membrane, making it porous and leaky. This allows two additional proteins called Smax and cytochrome C to spill into the cytool.

Smax binds the proteins that normally inhibit apoptosis and deactivates them. Meanwhile, cytochrome C binds to both ATP, the main form of intracellular energy, as well as an enzyme called APAF 1. Together, cytochrome C and APAF 1 combine to form a large protein complex called apoptosome. The apath 1 portion of the apoptosome then cleaves an enzyme called procaps 9 into its active form capsace 9. Capsace 9 then goes on to activate capsace 3 and capsace 3 goes on to activate other capsacases like a chain event. Eventually this caps cascade leads a cell to commit apoptosis.

That's because these capsacases cleave the proteins that make up the cell's nucleus, organels, and cytokeleton. A bit like a ninja sabotaging a bridge by removing its nuts and bolts. This destroys the cytokeleton as well as the proteins that anchor the cytokeleton to the cell membrane. As a result, the cell membrane starts to develop blebs or bulges in the cell membrane. The blebs are structurally weak, so they start to break off from the cell membrane, eventually forming small apoptoic bodies that are eaten by neighboring fagosites.

At the same time, the apoptotic cell releases anti-inflammatory signals, thereby preventing the recruitment of other immune cells from the blood and preventing tissue inflammation. So, apoptosis is a neat process that conveniently recycles the organic contents of the dead cell. Now when the signals from apoptosis come from outside the cell, it's called the extrinsic pathway. One example is when a nearby macrofase recognizes an old cell, a pathogenic cell or a cell that has completed its task. In these situations, a macrofase can initiate apoptosis by releasing tumor necrosis factor alpha or TNF alpha, a cell signaling protein.

that binds to very appropriately named death receptors on the target cell membrane. One example being tumor necrosis factor receptor 1. The systolic end of this receptor dives deep inside the cell and it's called the death domain. When the TNF alpha binds to the tumor necrosis factor receptor 1, the death domain changes its shape and is able to bind to two proteins. One is called fast associated protein with death domain or FAD and the other is called tumor necrosis factor receptor type one associated death domain protein or TR AD.

So the death receptor FAD and TR AD come together to form a multicomplex protein called wait for it the deathinducing signal complex or disk. Once everything is together disk cleaves procaps 8 into capsace 8 which in turn activates capsace 3 and capsace 3 goes on to activate other capsacases. This initiates the capsace cascade that commits the cell to apoptosis. After that, the process of apoptosis unfolds just like the intrinsic pathway. Now in addition to macrofasages if a cytotoxic TE-C cell detects that a cell is expressing foreign antigens the T- cell will express a protein on its membrane called fast lian which binds to a death receptor on the target cell called the first apoptosis signal receptor or fast receptor. Similar to the death domain of tumor necrosis factor receptor 1, the fast receptor protein also has its very own death domain that can bind to FAD to form disk. As before, disk activates procaps

8 into capsace 8 and that triggers the capsace cascade which leads to apoptosis. All right, let's switch gears and take a look at necrosis which can be triggered by external factors like an infection or extremely hot or cold temperatures as well as internal factors like tissue eskeeia. Now there are three main types of necrosis called primary, secondary and regulated necrosis. Primary necrosis, also known as accidental necrosis or onotic necrosis, typically occurs when eskeeia disrupts the normal functioning of mitochondria.

As a result, the cell is unable to synthesize ATP, causing all ATP dependent cellular processes to stop working, including the ionic pumps that regulate the flow of ions in and out of the cell. Without functioning ion pumps, sodium starts to flow into the cell and it's followed by water. This causes the cell to swell up like a balloon. This process of cell swelling is called enkosis. Soon the cell bursts and spills its internal contents and small molecules called damage associated molecular patterns into the surroundings. These molecules trigger the inflammatory response and attract nearby immune cells to release substances like proteases, which are enzymes that degrade proteins, and reactive oxygen species, which are unstable molecules that can damage other cells. If this inflammatory process occurs among enough cells, it can destroy the tissue. And if it happens on a massive level, it can lead to organ

dysfunction. Now, it turns out that primary necrosis comes in a few different flavors. First, there's coagulative necrosis, which occurs when a tissue becomes hypoxic, has low levels of oxygen, most commonly due to eskeeia. Hypoxia causes structural proteins to bend out of shape, like twisting a paperclip so that it can no longer work. Hypoxia also affects lossal enzymes which become ineffective at getting rid of the affected proteins. So although the cells die, they retain some structure and don't get completely destroyed.

From a macroscopic level, the dead tissue becomes a gel-like substance and has a pale wedge shape with the apex oriented toward the obstruction. That's because a blood vessel typically serves a region of tissue that typically fans out and all of that tissue becomes hypoxic and then underos coagulative necrosis. Occasionally blood re-enters the area of necro tissue like if a blocked blood vessel opens back up and when that happens it gives the tissue a dark red color and it's called a red infart. Coagulative necrosis can occur in any cell of the body, but it occurs most often when there's low oxygen to the heart, kidneys, or spleen tissue.

Next, there's liquefosis that occurs when hydraytic enzymes completely digest the dead cells into a creamy substance full of dead immune cells. Think of a cream fil donut. Liqueactive necrosis is most commonly seen in the brain. However, it can also happen to pancreatic cells or within an abscess located anywhere in the body. The brain has resident macrofasages called microgal cells that contain hydraytic enzymes. These enzymes completely destroy damaged brain cells basically liquefying the dead brain tissue. Similarly, the pancreas has various enzymes like trison that are designed to digest food but sometimes get activated in chronic inflammation due to gallstones or alcohol consumption and destroy the pancreatic tissue itself.

Finally, in abscesses, neutrfils use their proteolytic enzymes to liquefy tissue which results in pus. Next there's gangrous necrosis and it also occurs due to hypoxia. So that's why some consider it a form of coagulative necrosis. Gangrous necrosis typically affects the lower limbs and gastrointestinal tract and it causes the tissue to get dried up like a mummy. Sometimes called dry gangrine. But if the dry gangrine gets infected then liquefosis can occur and then it's called wet gang. Next, there's cas necrosis, and it's a bit of a mix between coagulative and liquefiive necrosis. Typically, it's the result of a fungal or mcoacterial infection. Classically, mcoacterium tuberculosis, which causes tuberculosis.

The dead cells disintegrate but are not fully digested, which leaves the tissue with a cottage cheese consistency. Next, there's fat necrosis, which most commonly occurs when there's trauma to fatty organs that have a lot of atapost cells like the pancreas or the breasts. Trauma to the pancreas or the breasts rupture the atapost cell membranes, which makes them spill their fatty acids into extracellular space. There, the fatty acids combine with calcium, which leads to distrophic calcifications in the tissue that look like bits of chalk in the tissue.

Now in addition the pancreas can also undergo fat necrosis as a result of inflammation called pancreatitis. With pancreatitis the pancreatic cells spill lipase around the pancreas. Lipase helps digest fats. So it causes fatty acids to spill out of the fatty retroparitinal tissue that's adjacent to the pancreas. Finally, there's fibroid necrosis which is almost always found in malignant hypertension and vasculitis. With hypertension, a constant high blood pressure damages the muscular wall of the small arteries. So, fibbrin, a protein involved in the clotting of blood, starts to infiltrate and damage the walls of the damaged blood vessels.

Similarly, in vasculitis, there's an inflammatory reaction in the blood vessel walls that causes destruction. Now, let's take a look at secondary necrosis, which occurs when there are no fagosites to clean up the mess of an apoptoic cell. As a result, the cell membrane of an apoptotic cell loses integrity and releases internal contents into the surroundings. In contrast to primary necrosis where damage associated molecular patterns induce a strong inflammatory response during secondary necrosis apoptoic cells release modified damaged associated molecular patterns that typically result in chronic inflammation.

Finally, there are regulated or programmed types of necrosis such as necropsis, pyropysis, and feropticis. Regulated necrosis is defined as genetically controlled cell death characterized by hallmarks of primary necrosis such as cellular swelling and leakage of intracellular contents. Regulated necrosis triggers a stronger immune response when compared to apoptosis but weaker when compared to primary necrosis. All right, as a quick recap, apoptosis is a commonly occurring form of programmed cell death whereas necrosis is a less common process where cells die due to injury or disease.

Apoptosis occurs due to intrinsic and exttrinsic pathways. With apoptosis, white blood cells come in and clean up the dead tissue. So, this is a neat way for cells to die. Necrosis occurs because of external factors like an infection as well as internal factors like tissue eskemia. There are three main types of necrosis and they include primary, secondary and regulated necrosis. Primary necrosis includes six types of necrosis. Coagulative and gangrinous necrosis which happened to hypoxic tissues. Liquifactive necrosis which happens because of hydraytic enzymes. Casius necrosis like in tuberculosis.

Fat necrosis which happens when fatty acids spill outside atapost cells like during trauma. And finally fibbronoid necrosis which is caused by fibbrin deposits like in malignant hypertension. On the flip side, secondary necrosis occurs when there are no fagosytes to clean up the mess of an apoptoic cell. While regulated necrosis refers to a genetically controlled cell death characterized by cellular swelling and leakage of intracellular components,

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Questions about this episode

What is discussed in "Necrosis and apoptosis"?

In order: 0:00 apoptosis, necrosis; 3:00 apoptosis, necrosis, tumor necrosis factor alpha, tumor necrosis factor receptor 1; 6:00 necrosis, apoptosis, coagulative necrosis, tumor necrosis factor receptor 1; 9:00 necrosis, coagulative necrosis; 12:00 necrosis, apoptosis, fat necrosis; 15:00 necrosis, fat necrosis.

What is mentioned in this Osmosis from Elsevier episode?

11 people, works and ideas are mentioned, including necrosis, apoptosis, capsase, coagulative necrosis, fat necrosis, ischemia. Each one on this page links to its own page with every episode that mentions it.

How long is "Necrosis and apoptosis"?

The episode runs 17 min; the transcript is about 2,055 words in 21 timestamped sections.

More from Osmosis from Elsevier

About this transcript: the episode's spoken words as captioned on YouTube, split into timestamped sections. Reclip.Me locates every person, work and idea in the text, keeps the time it is first named, and quotes the words around it verbatim. Last updated January 24, 2026.