Podcast
Questions and Answers
What type of damage can occur to DNA as a result of exposure to various agents?
What type of damage can occur to DNA as a result of exposure to various agents?
- Temporary damage
- Repairable damage
- Irreparable damage (correct)
- Reversible damage
What is one site where protein synthesis occurs and can be affected by damage?
What is one site where protein synthesis occurs and can be affected by damage?
- Golgi Apparatus
- Nucleus
- Mitochondria
- Endoplasmic Reticulum (ER) (correct)
What is the structure that provides scaffolding and 'motor' functions for cells?
What is the structure that provides scaffolding and 'motor' functions for cells?
- Cytoskeleton (correct)
- Nucleolus
- Cytoplasm
- Cell Membrane
What is the process by which cells undergo programmed cell death?
What is the process by which cells undergo programmed cell death?
What are the cellular components that suffer damage upon exposure to various agents?
What are the cellular components that suffer damage upon exposure to various agents?
What is the term for the process of protein synthesis that occurs after transcription?
What is the term for the process of protein synthesis that occurs after transcription?
What is the term used to describe the process of self-eating in cells?
What is the term used to describe the process of self-eating in cells?
What is the main difference between autophagy and necrosis?
What is the main difference between autophagy and necrosis?
What is the term used to describe the appearance of cells undergoing autophagy?
What is the term used to describe the appearance of cells undergoing autophagy?
What is the purpose of autophagy in cells?
What is the purpose of autophagy in cells?
What happens to the cellular components during autophagy?
What happens to the cellular components during autophagy?
What is the role of lysosomes in autophagy?
What is the role of lysosomes in autophagy?
What is the consequence of impaired autophagy?
What is the consequence of impaired autophagy?
What is the term used to describe the condensed chromatin in cells undergoing autophagy?
What is the term used to describe the condensed chromatin in cells undergoing autophagy?
What is the result of damage to lysosomal membranes?
What is the result of damage to lysosomal membranes?
What is the primary source of energy for energy-dependent cellular functions?
What is the primary source of energy for energy-dependent cellular functions?
What is the consequence of damage to cellular membranes?
What is the consequence of damage to cellular membranes?
Which of the following can cause DNA damage?
Which of the following can cause DNA damage?
What is the result of necrosis?
What is the result of necrosis?
Which of the following is a consequence of radiation?
Which of the following is a consequence of radiation?
What is the result of apoptosis?
What is the result of apoptosis?
What is the consequence of hypoxia/ischemia?
What is the consequence of hypoxia/ischemia?
What is the function of the sensors in the ER membrane?
What is the function of the sensors in the ER membrane?
What happens when the amount of misfolded proteins is too great to be corrected?
What happens when the amount of misfolded proteins is too great to be corrected?
What is the purpose of the unfolded protein response?
What is the purpose of the unfolded protein response?
What type of proteins are involved in detecting misfolded proteins in the ER?
What type of proteins are involved in detecting misfolded proteins in the ER?
What is the outcome of the terminal unfolded protein response?
What is the outcome of the terminal unfolded protein response?
Where do the sensors that detect misfolded proteins reside?
Where do the sensors that detect misfolded proteins reside?
What is the result of defective DNA repair?
What is the result of defective DNA repair?
What is the consequence of mutations in DNA replication?
What is the consequence of mutations in DNA replication?
What is the role of insulin/IGF signaling in cellular aging?
What is the role of insulin/IGF signaling in cellular aging?
What is the result of decreased protein synthesis?
What is the result of decreased protein synthesis?
What is the consequence of cellular protein accumulation?
What is the consequence of cellular protein accumulation?
What is the role of TOR in cellular aging?
What is the role of TOR in cellular aging?
What is the result of decreased cell functions?
What is the result of decreased cell functions?
What is the consequence of altered transcription?
What is the consequence of altered transcription?
DNA damage can be repaired in cells.
DNA damage can be repaired in cells.
The endoplasmic reticulum (ER) is involved in post-translational protein processing.
The endoplasmic reticulum (ER) is involved in post-translational protein processing.
Cytoskeleton is responsible for scaffolding and motor functions in cells.
Cytoskeleton is responsible for scaffolding and motor functions in cells.
Apoptosis is a type of programmed cell death.
Apoptosis is a type of programmed cell death.
Lysosomes are involved in protein synthesis.
Lysosomes are involved in protein synthesis.
Autophagy is a process of cellular self-eating.
Autophagy is a process of cellular self-eating.
Superoxide is converted to hydrogen peroxide spontaneously and by the action of the enzyme superoxide dismutase.
Superoxide is converted to hydrogen peroxide spontaneously and by the action of the enzyme superoxide dismutase.
The degree of injury from any injurious stimulus always remains the same.
The degree of injury from any injurious stimulus always remains the same.
Intermediates are generated when oxygen is only partially reduced.
Intermediates are generated when oxygen is only partially reduced.
The production of misfolded proteins can increase the production of normal proteins.
The production of misfolded proteins can increase the production of normal proteins.
Cellular injury and death are always irreversible.
Cellular injury and death are always irreversible.
Telomerase is an enzyme that can repair DNA damage.
Telomerase is an enzyme that can repair DNA damage.
Mutations can result in the production of abnormal proteins.
Mutations can result in the production of abnormal proteins.
Hydrogen peroxide is a reactive oxygen species that can cause cellular damage.
Hydrogen peroxide is a reactive oxygen species that can cause cellular damage.
Superoxide dismutase is an enzyme that converts hydrogen peroxide to water and oxygen.
Superoxide dismutase is an enzyme that converts hydrogen peroxide to water and oxygen.
Enzymes are responsible for repairing DNA mutations.
Enzymes are responsible for repairing DNA mutations.
The extent of cellular injury depends on the severity of the injurious stimulus.
The extent of cellular injury depends on the severity of the injurious stimulus.
The accumulation of misfolded proteins can lead to cell death.
The accumulation of misfolded proteins can lead to cell death.
Reactive oxygen species are always beneficial to cellular metabolism.
Reactive oxygen species are always beneficial to cellular metabolism.
Cell injury can result from abnormalities in one or more essential cellular components.
Cell injury can result from abnormalities in one or more essential cellular components.
Decreased protein synthesis can lead to cellular aging.
Decreased protein synthesis can lead to cellular aging.
Autophagy is a process that occurs in response to DNA damage.
Autophagy is a process that occurs in response to DNA damage.
The enzyme myeloperoxidase is responsible for converting hypochlorous acid into a reactive compound.
The enzyme myeloperoxidase is responsible for converting hypochlorous acid into a reactive compound.
Impaired autophagy can lead to inflammation and tissue damage.
Impaired autophagy can lead to inflammation and tissue damage.
The progression of cellular aging is influenced by the rate of telomere shortening.
The progression of cellular aging is influenced by the rate of telomere shortening.
Mitochondria are not involved in the process of cell injury.
Mitochondria are not involved in the process of cell injury.
Hypoxia can lead to cell injury by causing oxidative stress and mitochondrial dysfunction.
Hypoxia can lead to cell injury by causing oxidative stress and mitochondrial dysfunction.
The nucleus is not a site of protein synthesis.
The nucleus is not a site of protein synthesis.
Inflammation is a consequence of impaired autophagy.
Inflammation is a consequence of impaired autophagy.
Cell injury can occur due to abnormalities in the lysosomal membrane.
Cell injury can occur due to abnormalities in the lysosomal membrane.
Calorie restriction can activate various signaling pathways and transcription factors that counteract cellular aging.
Calorie restriction can activate various signaling pathways and transcription factors that counteract cellular aging.
Reactive oxygen species (ROS) are involved in promoting cellular aging.
Reactive oxygen species (ROS) are involved in promoting cellular aging.
The target of rapamycin (TOR) is a signaling pathway that promotes cellular aging.
The target of rapamycin (TOR) is a signaling pathway that promotes cellular aging.
Decreased protein synthesis can lead to cellular protein accumulation.
Decreased protein synthesis can lead to cellular protein accumulation.
Insulin-like growth factor (IGF) signaling is involved in promoting cellular aging.
Insulin-like growth factor (IGF) signaling is involved in promoting cellular aging.
DNA damage can cause cardiovascular disease.
DNA damage can cause cardiovascular disease.
Replicative senescence is a mechanism of cellular aging caused by telomere shortening.
Replicative senescence is a mechanism of cellular aging caused by telomere shortening.
Defective protein homeostasis can lead to cardiovascular disease.
Defective protein homeostasis can lead to cardiovascular disease.
What is the characteristic feature of apoptotic cells' nuclei?
What is the characteristic feature of apoptotic cells' nuclei?
What is the effect of the preparative regimen for colonoscopy on epithelial cells?
What is the effect of the preparative regimen for colonoscopy on epithelial cells?
What type of molecules are free radicals?
What type of molecules are free radicals?
What is the term used to describe the process of cellular self-eating?
What is the term used to describe the process of cellular self-eating?
What is the consequence of radiation on cells?
What is the consequence of radiation on cells?
What are the primary cellular targets of injurious stimuli?
What are the primary cellular targets of injurious stimuli?
What is the role of reactive oxygen species (ROS) in cellular damage?
What is the role of reactive oxygen species (ROS) in cellular damage?
What is the characteristic feature of apoptotic cells' bodies?
What is the characteristic feature of apoptotic cells' bodies?
What type of damage can reactive oxygen species (ROS) cause?
What type of damage can reactive oxygen species (ROS) cause?
What is the consequence of ATP depletion in cells?
What is the consequence of ATP depletion in cells?
What is the normal process by which molecular oxygen is reduced to generate water during mitochondrial respiration?
What is the normal process by which molecular oxygen is reduced to generate water during mitochondrial respiration?
What is the consequence of impaired autophagy?
What is the consequence of impaired autophagy?
What is the result of ischemia/hypoxia?
What is the result of ischemia/hypoxia?
What is the result of impaired reduction of molecular oxygen during mitochondrial respiration?
What is the result of impaired reduction of molecular oxygen during mitochondrial respiration?
What is the site where reactive oxygen species (ROS) are normally produced in small amounts during mitochondrial respiration?
What is the site where reactive oxygen species (ROS) are normally produced in small amounts during mitochondrial respiration?
What is the role of enzymes such as glutathione peroxidase in cells?
What is the role of enzymes such as glutathione peroxidase in cells?
What is the consequence of nuclear DNA damage?
What is the consequence of nuclear DNA damage?
What is the consequence of the accumulation of reactive oxygen species (ROS) in cells?
What is the consequence of the accumulation of reactive oxygen species (ROS) in cells?
What is the primary source of energy for energy-dependent cellular functions?
What is the primary source of energy for energy-dependent cellular functions?
What is the result of cellular membrane damage?
What is the result of cellular membrane damage?
What is the normal process that occurs during mitochondrial respiration to generate energy?
What is the normal process that occurs during mitochondrial respiration to generate energy?
What is the result of injury due to hypoxia?
What is the result of injury due to hypoxia?
What is the role of enzymes in the reduction of molecular oxygen during mitochondrial respiration?
What is the role of enzymes in the reduction of molecular oxygen during mitochondrial respiration?
What is the consequence of mitochondrial damage?
What is the consequence of mitochondrial damage?
What is the role of superoxide in cellular injury?
What is the role of superoxide in cellular injury?
What is the result of the incomplete reduction of molecular oxygen during mitochondrial respiration?
What is the result of the incomplete reduction of molecular oxygen during mitochondrial respiration?
What is the consequence of impaired oxidative phosphorylation?
What is the consequence of impaired oxidative phosphorylation?
What is the primary function of mitochondrial respiration?
What is the primary function of mitochondrial respiration?
What is the result of radiation?
What is the result of radiation?
What is the role of oxidative phosphorylation in cellular function?
What is the role of oxidative phosphorylation in cellular function?
What is the consequence of mitochondrondrial damage?
What is the consequence of mitochondrondrial damage?
What is the result of ischemia?
What is the result of ischemia?
What happens to cellular components when the ER membrane is damaged, leading to a decline in protein synthesis?
What happens to cellular components when the ER membrane is damaged, leading to a decline in protein synthesis?
How does p53 respond to damaged DNA?
How does p53 respond to damaged DNA?
What is the purpose of DNA repair mechanisms?
What is the purpose of DNA repair mechanisms?
What happens to cells when the unfolded protein response is triggered?
What happens to cells when the unfolded protein response is triggered?
What is the outcome of defective DNA repair?
What is the outcome of defective DNA repair?
What is the role of the unfolded protein response in cellular aging?
What is the role of the unfolded protein response in cellular aging?
What is the consequence of impaired autophagy?
What is the consequence of impaired autophagy?
What is the role of p53 in regulating cellular aging?
What is the role of p53 in regulating cellular aging?
The generation of ______ is increased by exposure to reversible injury but larger doses of the toxin or more prolonged ischemia.
The generation of ______ is increased by exposure to reversible injury but larger doses of the toxin or more prolonged ischemia.
UV light, ______ and toxins, and during normal cellular aging, may cause necrosis.
UV light, ______ and toxins, and during normal cellular aging, may cause necrosis.
Stretched muscle in the leg survives ______ for 2 hours.
Stretched muscle in the leg survives ______ for 2 hours.
Oxygen deprivation for 3 hours, whereas cardiac muscle, which has higher metabolic needs, dies.
Oxygen deprivation for 3 hours, whereas cardiac muscle, which has higher metabolic needs, dies.
This also leads to ROS production because of incomplete ______ of oxygen.
This also leads to ROS production because of incomplete ______ of oxygen.
The genetic makeup of the individual may also determine the reaction to ______ agents.
The genetic makeup of the individual may also determine the reaction to ______ agents.
The human body needs to burn ___________ kg of ATP every day.
The human body needs to burn ___________ kg of ATP every day.
After 20 to 30 minutes of ______, the gene expression of the individual.
After 20 to 30 minutes of ______, the gene expression of the individual.
Ischemia is a condition of ___________ deprivation.
Ischemia is a condition of ___________ deprivation.
This may also determine the reaction to ______ and further damage to cellular components.
This may also determine the reaction to ______ and further damage to cellular components.
Damages to ATP can cause ___________ to many cellular components.
Damages to ATP can cause ___________ to many cellular components.
Insulin/ ______ signaling plays a role in cellular aging.
Insulin/ ______ signaling plays a role in cellular aging.
Defective ______ repair can lead to cellular aging.
Defective ______ repair can lead to cellular aging.
The reduction of ATP-dependent Na-K pump activity results in ___________ influx of Na and water.
The reduction of ATP-dependent Na-K pump activity results in ___________ influx of Na and water.
The ER is affected by the reduction of ATP-dependent Na-K pump activity, leading to ___________ and dilation.
The ER is affected by the reduction of ATP-dependent Na-K pump activity, leading to ___________ and dilation.
Mutations in ______ replication can lead to misfolded proteins.
Mutations in ______ replication can lead to misfolded proteins.
Accumulation of cellular proteins can lead to ______ cellular functions.
Accumulation of cellular proteins can lead to ______ cellular functions.
The reduction of ATP-dependent Na-K pump activity can cause ___________ and damage to the ER.
The reduction of ATP-dependent Na-K pump activity can cause ___________ and damage to the ER.
______ signaling can counteract cellular aging.
______ signaling can counteract cellular aging.
The ATP-dependent Na-K pump plays a crucial role in maintaining the ___________ of the plasma membrane.
The ATP-dependent Na-K pump plays a crucial role in maintaining the ___________ of the plasma membrane.
Hypoxia and ___________ can cause damage to ATP and affect cellular functions.
Hypoxia and ___________ can cause damage to ATP and affect cellular functions.
Altered ______ can lead to cellular aging.
Altered ______ can lead to cellular aging.
Cellular protein accumulation can lead to ______ cellular proteins.
Cellular protein accumulation can lead to ______ cellular proteins.
Decreased protein synthesis can lead to ______ cellular functions.
Decreased protein synthesis can lead to ______ cellular functions.
In some cases, pers ______ pa ______ o ______ c med ______ ors, such as ______ hormone-induced ______ of the breast, and ______ hyperp ______ sia, affect ______ end ______ rium.
In some cases, pers ______ pa ______ o ______ c med ______ ors, such as ______ hormone-induced ______ of the breast, and ______ hyperp ______ sia, affect ______ end ______ rium.
______ stress can cause ______ in bone and muscle cells.
______ stress can cause ______ in bone and muscle cells.
______ adaptations are responses to mutations and oncogenic ______ formation.
______ adaptations are responses to mutations and oncogenic ______ formation.
______ allows cells to ______ their structure and function and thus ______.
______ allows cells to ______ their structure and function and thus ______.
______ is a decrease in the number of cells and, hence, may cause an ______ injury.
______ is a decrease in the number of cells and, hence, may cause an ______ injury.
______ and organ ______ can occur as a result of ______ function.
______ and organ ______ can occur as a result of ______ function.
______ injury can occur at the expense of normal ______ function.
______ injury can occur at the expense of normal ______ function.
______ is caused by ______ normal function, leading to ______ injury.
______ is caused by ______ normal function, leading to ______ injury.
Hyperp_______a can be psychological or pathological and, in naming by insulin-like growth factor, so cells cycle less and suffer boon_______s and suffer various biochemical sous_______ons.
Hyperp_______a can be psychological or pathological and, in naming by insulin-like growth factor, so cells cycle less and suffer boon_______s and suffer various biochemical sous_______ons.
Grow_______ factors are produced by a variety of cell types. Pos_______orum
Grow_______ factors are produced by a variety of cell types. Pos_______orum
In addition to these intrinsic abnormalities, damaged and dying en_______g________nt of the breast due to increased production of ductular cells induce low-_______ inflammation, and chronic inflammation pre-
In addition to these intrinsic abnormalities, damaged and dying en_______g________nt of the breast due to increased production of ductular cells induce low-_______ inflammation, and chronic inflammation pre-
Grow_______ factors are responsible for stimulating production of ductular cells and, and some types of cancer.
Grow_______ factors are responsible for stimulating production of ductular cells and, and some types of cancer.
Surviving cells after death or removal of some of the cells in an organ is called comp_______satory _________a.
Surviving cells after death or removal of some of the cells in an organ is called comp_______satory _________a.
Damaged and dying cells can induce _________ inflammation, and chronic inflammation pre-.
Damaged and dying cells can induce _________ inflammation, and chronic inflammation pre-.
Grow_______ factors are responsible for stimulating production of ductular cells and, and some types of _________.
Grow_______ factors are responsible for stimulating production of ductular cells and, and some types of _________.
Hyperp_______a can be psychological or pathological and, in naming by _________-like growth factor, so cells cycle less and suffer boon_______s and suffer various biochemical sous_______ons.
Hyperp_______a can be psychological or pathological and, in naming by _________-like growth factor, so cells cycle less and suffer boon_______s and suffer various biochemical sous_______ons.
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Study Notes
Autophagy
- Autophagy is a form of "self-eating" (Greek, phaga = to eat) where cells digest their own organelles and recycle them to provide energy for survival.
- In H&E-stained sections, the nucleus appears materlike to provide energy for survival.
Autophagy vs. Necrosis
- Autophagy differs from necrosis in that cells survive by recycling their own organelles.
- In necrosis, cells die due to irreversible damage.
- In H&E-stained sections, autophagic cells appear with shrunken, pyknotic nuclei, and vacuoles containing cellular debris.
Cellular Components and Damage
- Other cellular components that suffer damage upon exposure to various injurious agents include:
- Endoplasmic Reticulum (ER) involved in protein synthesis and post-translational processing
- Cytoskeleton providing structural support and motor functions
- Mitochondria responsible for energy production
- Cellular membranes vulnerable to leakage and damage
Mechanisms of Cell Injury and Death
- Hypoxia/ischemia, radiation, and other injurious agents can cause cell injury and death.
- Mitochondrial damage leads to reduced ATP production, increased ROS, and activation of caspases, ultimately resulting in apoptosis.
- DNA damage triggers apoptosis, while mutations can lead to cellular aging and death.
- ER stress triggers an unfolded protein response, which can protect the cell from misfolded proteins or induce apoptosis if the damage is irreversible.
Cell Death Pathways
- Necrosis: irreversible cell damage and death
- Apoptosis: programmed cell death in response to internal or external signals
- Autophagy: self-eating and recycling of cellular components to provide energy for survival
Mechanisms of Cell Injury and Death
- Irreparable DNA damage can occur due to exposure to various injurious agents, leading to cellular injury and death.
- Other cellular components, such as the ER and cytoskeleton, can also suffer damage upon exposure to injurious agents.
Cellular Components Prone to Damage
- Mitochondria, membranes, and the nucleus are essential cellular components that can be damaged, leading to cellular injury and death.
- The degree of injury from any stimulus varies depending on the degree of abnormality in one or more of these essential cellular components.
Mechanisms of DNA Damage
- Superoxide, a reactive oxygen species, can be converted to hydrogen peroxide (H2O2) spontaneously or by the action of the enzyme superoxide dismutase.
- Hydrogen peroxide can be converted to a highly reactive compound, hypochlorous acid, by the enzyme myeloperoxidase present in leukocyte granules.
- This reactive compound can cause DNA damage and disrupt cellular function.
Consequences of Cellular Damage
- Decreased cell replication due to progressive loss of cellular function can lead to tissue damage and organ injury.
- Abnormalities in cellular components can lead to increased production of misfolded proteins, which can accumulate and cause cellular damage.
- Decreased telomerase activity, which maintains telomere length, can lead to cellular senescence and aging.
Aging and Cellular Damage
- DNA damage, replicative senescence, and decreased and misfolded proteins are among the best-described mechanisms of cellular aging.
- Environmental stresses, such as calorie restriction, can counteract aging by activating various signaling pathways and transcription factors.
- Cellular aging can lead to tissue damage and organ injury, and can also increase the risk of age-related diseases.
Apoptotic Cells and Free Radicals
- Apoptotic cells in the colonic epithelium are shown, which are induced by the preparative regimen for colonoscopy.
- Free radicals are highly reactive molecules that can cause apoptosis in epithelial cells.
- Apoptotic cells are characterized by fragmented nuclei, condensed chromatin, and shrunken cell bodies.
Free Radicals and ROS
- ROS (Reactive Oxygen Species) are produced normally in small amounts in cells during redox reactions.
- ROS are highly reactive molecules that can cause oxidative damage to cellular components.
- ROS include oxygen radicals, such as superoxides, hydroxyl radicals, and hydrogen peroxide.
Mitochondria and ROS
- Mitochondria are the sites where ATP is produced, and ROS are produced as a byproduct.
- ROS can damage mitochondrial components, leading to the production of more ROS.
- Mitochondrial dysfunction can lead to the release of ROS, which can cause apoptosis.
Cellular Targets of Injurious Stimuli
- Most injurious stimuli affect mitochondria, cellular membranes, or nuclear DNA.
- Injury to these structures can progress to necrosis or apoptosis.
- ATP, adenosine triphosphate, is a key player in cellular energy metabolism.
ROS and Cellular Damage
- ROS can damage lipids, proteins, and DNA, leading to cellular damage.
- Peroxidation of lipids, oxidation of proteins, and breaks in DNA can occur due to ROS.
- ROS can also affect cellular components, such as enzymes, and lead to the accumulation of damaged proteins.
DNA Damage and Repair
- Damaged DNA can activate p53, which arrests the cell cycle in the G1 phase to allow for DNA repair.
- DNA repair mechanisms can correct DNA damage, but if the damage is severe, p53 can trigger apoptosis.
- The accumulation of DNA damage can lead to the activation of DNA repair mechanisms, which can prevent further damage.
Cellular Response to Damage
- Cells can respond to damage by activating repair mechanisms or undergoing apoptosis.
- The choice between repair and apoptosis depends on the severity of the damage and the cellular context.
- Apoptosis is a mechanism to eliminate damaged cells, which can prevent further damage to the organism.
Ischemia and Oxidative Stress
- Ischemia leads to oxygen deprivation, which increases oxidative stress and ROS production.
- This causes damage to cellular components, including the plasma membrane, and disrupts ATP-dependent Na-K pumps.
Cellular Effects
- Reduced cellular activity and ATP production occur due to oxidative stress.
- Decreased ATP production damages many cellular components, leading to:
- Reduced activity of the plasma membrane ATP-dependent Na-K pump.
- Influx of Na and water, causing cell swelling and damage.
- Disruption of ER function, leading to protein misfolding and aggregation.
Genetic Effects
- Oxidative stress and DNA damage lead to:
- Mutations in DNA replication.
- Defective DNA repair.
- Altered gene transcription.
Cellular Aging
- Decreased cellular function and increased DNA damage contribute to cellular aging.
- Counteracting cellular aging requires maintaining protein homeostasis and promoting DNA repair.
Hyperplasia
- Hyperplasia can be physiological or pathological and is induced by growth factors.
- It can lead to increased cell proliferation and protein synthesis.
- Examples of hyperplasia include:
- Insulin/IGF signaling pathway.
- TOR pathway.
- Hormone-induced hyperplasia.
Pathological Consequences
- Hyperplasia can lead to various diseases, including:
- Atherosclerosis.
- Type 2 diabetes.
- Cancer.
- It can also cause chronic inflammation and tissue damage.
Compensatory Mechanisms
- Compensatory mechanisms, such as hyperplasia, can occur in response to tissue damage or stress.
- Examples include:
- Compensatory hyperplasia in response to hormonal changes.
- Compensatory hyperplasia in response to mechanical stress.
Cellular Damage and Necrosis
- Damage to cell membranes can lead to the release of enzymes, causing cell injury and necrosis
- ROS (Reactive Oxygen Species) can damage cell membranes, leading to cell injury and necrosis
- Plasma membrane damage can result in cell death, leading to necrosis
Nuclear Damage
- Nuclear DNA is damaged, disrupting transcription-dependent cellular functions (e.g., protein synthesis)
- Nuclear damage can disrupt gene expression, leading to cell injury and death
ROS Production
- ROS are produced normally in small amounts during cellular respiration and metabolism
- ROS can trigger apoptosis (cell death) by damaging mitochondria
- Increased ROS production can contribute to coronary artery disease and stroke
Cellular Response to Injury
- Hypoxia and ischemia can lead to reduced ATP production, causing energy-dependent cellular systems to fail
- Cellular swelling, loss of microvilli, and bleb formation can occur in response to injury
- ER swelling and increased ROS production can exacerbate tissue injury
Consequences of Cellular Injury
- Accumulation of mutations in DNA can occur naturally and can be enhanced by ROS and environmental mutagens
- Influx of calcium and sodium ions can contribute to cellular injury and death
- Efflux of potassium ions can lead to cellular injury and death
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Description
Learn about autophagy, a process of self-eating, and its connection to apoptosis, a form of cell death. Understand the morphological appearance and distinct differences between these two cellular processes.
