Last Lecture: Repair And Healing Flashcards
Steps of inflammation
Recognition- where injury is coming from
Recruitment
Removal of offending agent
Guarding the place to make sure no other ofening agent come there
Repair /healing
What is tissue repair
State the four phases of tissue repair or healing
the restoration of tissue architecture and function after an injury.(you’re not just restoring the architecture or anatomy. You’re restoring the function as well)
-Damage and immediate response
-Inflammation phase
-Proliferation phase(repair or healing properly starts here)-
• Re-epithelialization
• Fibroplasia and Granulation Tissue Formation
• Angiogenesis
-Remodeling / Maturation phase
Tissue repair and healing can be used interchangeably What’s the difference between tissue repair and healing
Wound healing
• Healing is a tissue response that follows inflammation in response to injury and consists of replacement of dead/damaged tissue with viable tissue by varying extents of two processes:
• 1. replacement by regenerated cells (of same type) or
• 2. fibrous (scar) tissue.
The Aim is to regain partial or complete organ structure or function. Processes are complex but orderly.
The damage area is replaced by-
• Regeneration of host parenchymal cells.
• Repair or organization or formation of fibrous scar
Wound healing:
• Acute inflammation/Homeostasis.
• Migration and proliferation of parenchymal cells
• Formation of new blood vessels (angiogenesis)
• Synthesis of extracellular matrix
• Remodeling / Maturation
- Repair involves the recovery of tissue integrity, focusing on both parenchymal and connective tissues, which may result in regeneration or fibrosis.
- Healing includes repair but is specifically concerned with the re-establishment of the surface epithelium and the overall resolution of inflammation.
Your distinction between repair and healing can be further clarified as follows:
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Definition: Repair refers to the restoration of tissue integrity following an injury. This process can involve:
- Regeneration: The replacement of damaged parenchymal cells with cells of the same type, restoring normal tissue structure and function.
- Fibrosis: The formation of connective tissue (scar tissue) when regeneration is not possible, restoring structural integrity but often resulting in loss of original tissue function.
- Tissue Involved: Repair typically involves both the tissue parenchyma (functional cells of an organ) and the connective tissue (supportive framework), depending on the extent of the damage and the tissue’s regenerative capacity.
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Definition: Healing is the broader process that includes repair but also specifically involves the restoration of surface epithelium, which covers and protects tissues.
- Restoration of Surface Epithelium: Healing particularly emphasizes the re-establishment of the epithelial layer, which is crucial for protecting underlying tissues from infection and further injury.
- Inflammation and Resolution: Healing also encompasses the resolution of the inflammatory response and the re-establishment of homeostasis in the affected area.
- Tissue Involved: Healing mainly involves the surface epithelium but also includes the underlying connective tissue, particularly when the injury involves deeper layers.
Explain the two types or processes of tissue repair and two examples of these processes
Both of the above processes involve the proliferation or growth of cells and close interactions between cells and the extracellular matrix, ECM.
True or false
Two processes of repair
Regeneration
: replacement of damaged tissues (damage could be due to an infection or inflammation or direct injury)
Eg: hepatocytes, epithelial cells of the skin and intestines,mucosal lining of alimentary canal
Scar formation
• Connective tissue deposition
Eg: deposition of collagen in the lungs, liver, kidneys as a consequence of chronic inflammation
What type of collagen is mainly deposited in scar formation of the remodeling or maturation phase of repair or wound healing
In scar formation, Type I collagen is primarily deposited during the remodeling/maturation phase. This type of collagen provides the scar with strength and structure. Initially, in the early stages of healing, Type III collagen is deposited, but as the healing process progresses, it is replaced by the more robust Type I collagen, which constitutes the majority of the final scar tissue.
What is the function of ECM (Extracellular matrix) to repair processes
Cells that are about to proliferate are induced by growth factors. They provide proteins for growth factors for the processes
The extracellular matrix (ECM) plays a crucial role in the repair processes of tissue, providing structural support and regulating cellular behavior. Here’s how the ECM functions in tissue repair:
- Scaffold for Cell Migration: The ECM serves as a physical scaffold that supports the migration of cells into the wound site during the repair process. Cells like fibroblasts, endothelial cells, and epithelial cells use the ECM to move into the damaged area, where they contribute to tissue regeneration and repair.
- Framework for New Tissue Formation: The ECM provides a framework for the deposition of new extracellular components and for the organization of the regenerating tissue. This is essential for maintaining the structural integrity of the tissue during repair.
- Cell Proliferation and Differentiation: The ECM influences cell proliferation, differentiation, and survival. It interacts with cells through integrins and other receptors, sending signals that regulate gene expression and cellular functions. For example, the composition and stiffness of the ECM can determine whether cells proliferate or differentiate into specific types needed for tissue repair.
- Angiogenesis: The ECM plays a critical role in angiogenesis (the formation of new blood vessels), which is vital during the proliferation phase of healing. Components of the ECM, such as fibronectin and collagen, provide signals that stimulate endothelial cells to form new capillaries, ensuring that the repairing tissue receives an adequate blood supply.
- Degradation and Synthesis: During the repair process, the ECM is continuously remodeled. Matrix metalloproteinases (MMPs) degrade damaged ECM components, while fibroblasts and other cells synthesize new ECM proteins. This dynamic remodeling is essential for clearing damaged tissue and replacing it with newly synthesized ECM, which supports the maturation of the healing tissue.
- Scar Formation: The remodeling of the ECM also plays a significant role in scar formation. As the tissue matures, the initial ECM components, like Type III collagen, are gradually replaced by stronger components, such as Type I collagen. This transition helps form the fibrous scar tissue that replaces the damaged tissue.
- Reservoir for Growth Factors: The ECM binds and sequesters growth factors, which are released in a controlled manner to influence cell behavior during repair. For example, growth factors like transforming growth factor-beta (TGF-β) and vascular endothelial growth factor (VEGF) are stored in the ECM and released as needed to promote cell proliferation, differentiation, and angiogenesis.
- Signal Modulation: The ECM modulates the availability and activity of growth factors, ensuring that they are delivered to the right cells at the right time, thereby orchestrating the repair process efficiently.
The extracellular matrix (ECM) is integral to tissue repair, providing both structural support and biochemical signals that regulate cellular activities such as migration, proliferation, differentiation, and survival. It plays a central role in the repair process by organizing the regenerating tissue, facilitating angiogenesis, and undergoing dynamic remodeling to form scar tissue. The ECM’s interactions with cells and growth factors ensure that the repair process is well-coordinated and leads to the restoration of tissue integrity and function.
In what situations will a cell face regeneration and what situations will it face scar formation
Why will certain injuries cause scar formation ?
Regeneration:
Mild injury
Acute injury
Superficial injury
Scar formation:
Severe and chronic injury
Collagen is released by fibroblasts in the connective tissue
Severe and chronic injuries often result in scar formation due to several factors related to the nature and extent of the injury:
- Involves Larger Areas: Severe injuries typically damage a large area of tissue, including both the parenchymal (functional) cells and the underlying extracellular matrix (ECM). This extensive damage often exceeds the regenerative capacity of the tissue, necessitating repair through fibrosis (scar formation) rather than complete regeneration.
- Involves Multiple Tissue Layers: Severe injuries may affect multiple tissue layers or involve significant disruption of the tissue architecture, making it difficult for the original tissue to regenerate properly.
- Limited Cell Proliferation: Some tissues have a limited ability to regenerate. For example, cardiac muscle cells (myocytes) and neurons have very limited regenerative capacity. When these tissues are severely damaged, they are more likely to be replaced by scar tissue rather than functional cells.
- Loss of Parenchymal Cells: When parenchymal cells are lost or damaged beyond repair, they are often replaced by fibroblasts and collagen-producing cells that form scar tissue. Scar tissue lacks the specific functions of the original parenchymal cells.
- Persistent Inflammation: Chronic injuries lead to ongoing inflammation, which prolongs the inflammatory phase of healing. Continuous inflammation can lead to excessive fibroblast activation and collagen deposition, resulting in an accumulation of scar tissue.
- Increased Fibroblast Activity: Chronic inflammation stimulates fibroblasts to produce large amounts of collagen and other ECM components. Over time, this can lead to the formation of dense, fibrous scar tissue.
- Excessive ECM Production: In some cases, the repair process may involve the excessive production of ECM components, particularly collagen. This can result in the formation of thick, fibrous scar tissue that replaces the normal tissue structure.
- Disorganized Collagen Deposition: In severe or chronic injuries, the collagen matrix may be laid down in a disorganized manner, leading to scar tissue that is structurally and functionally different from the original tissue.
- Failure to Restore Original Architecture: Severe injuries often disrupt the normal tissue architecture, and the regenerative process may not fully restore the original structure. As a result, the tissue is replaced by scar tissue that lacks the functional organization of the original tissue.
Severe and chronic injuries cause scar formation because they often involve extensive damage that surpasses the regenerative capacity of the tissue, leading to the replacement of functional tissue with fibrous scar tissue. Chronic inflammation and abnormal healing responses contribute to excessive ECM production and disorganized collagen deposition, resulting in dense, fibrous scar tissue. This scar tissue provides structural support but often lacks the functional properties of the original tissue.
What are the three types of cells that proliferate during tissue repair or what types of cells are involved in tissue repair ?
What are the two things that influence how different types of tissues respond to injury or cell proliferation during tissue repair depends on what two things?
What are the three groups of tissues based on a cells ability to proliferate? Give three examples each of these three groups
Cell proliferation
Cells are in 3 groups depending on proliferative capacity:
Several cell types proliferate during tissue repair:
• Remnants of the injured tissues-These include surviving cells from the damaged tissue that can proliferate and contribute to repair if they are still functional and capable of dividing.
• Vascular endothelial cells-These cells proliferate to form new blood vessels (angiogenesis) at the area where proliferation will occur which is crucial for supplying the healing tissue with oxygen and nutrients.(cornea of eye and testes in males are the only places that blood doesn’t go there. They take nutrients from adjacent blood vessels)
• Fibroblasts-Fibroblasts proliferate to produce new extracellular matrix and collagen, which form the scaffold for new tissue and contribute to scar formation.
Depends on
• Capacity to proliferate
• Presence of tissue stem cells-Some tissues have stem cells that can differentiate into the required cell types for repair. The ability of stem cells to proliferate and differentiate is key to the tissue’s regenerative capacity.
This leads to three groups of tissues:
Labile-These tissues have a high turnover rate and continuously regenerate throughout life. They are capable of rapid cell division and repair. Labile cells, renewing cell population- continue to proliferate thru adult life. All epithelia, lymphoid and haemopoeitic cells.
Continuous replicators in cell cycle.
• Skin, vagina, cervix, salivary glands, uterus, urinary tract
Examples: • Skin: The epidermis is constantly renewed with cells from the basal layer. • Vagina: The epithelial lining is continuously replaced. • Cervix: The lining cells can regenerate rapidly. • Salivary Glands: They have a high capacity for regeneration. • Uterus: Endometrial lining is shed and regenerated during the menstrual cycle. • Urinary Tract: Epithelial cells in the urinary tract are continually replaced.
Stable-These tissues have a low to moderate turnover rate under normal conditions but can proliferate in response to injury or increased demand.they are in the G0 phase of the cell cycle. Stable cells, conditionally renewing cell population. Normally low rate of cell proliferation, but rapid burst in response to cell loss. E.g.
Parenchymal epithelial cells of all glands- hepatocytes, renal tubular epithelium, fibroblasts, chondrocytes, osteoblasts, endothelial cells, smooth muscle.
• Liver, kidney, pancreas, smooth muscles
Examples:
• Liver: Hepatocytes can regenerate after injury, though this is limited compared to labile tissues.
• Kidney: Tubular cells can regenerate to some extent, but the capacity is limited compared to labile tissues.
• Pancreas: Pancreatic cells can regenerate, but the process is slower and less efficient.
• Smooth Muscle: Can proliferate in response to injury or pathological conditions.
Permanent-These tissues have very limited or no capacity for regeneration. Damage to these tissues typically results in scar formation rather than functional tissue replacement. Permanent cells, static cell populations. Have no proliferative capacity during adult life. Eg neurones, striated muscle, cardiac muscle. Repair.
• Neurons, cardiac muscle
Examples:
• Neurons: Neurons in the central nervous system have very limited regenerative capacity, making damage often irreversible.
• Cardiac Muscle: Cardiac myocytes (heart muscle cells) have limited ability to regenerate after injury, leading to scar formation instead of functional tissue repair.
Skeletal Muscle Cells(there are some exceptions)
• Location: Skeletal muscles throughout the body.
• Function: Enable voluntary movements.
• Regeneration: Limited; extensive damage can lead to scar tissue rather than full muscle restoration.
4. Lens Epithelial Cells:
• Location: Lens of the eye.
• Function: Maintain lens transparency.
• Regeneration: Limited; damage can affect vision.
5. Hair Cells (in the Inner Ear):
• Location: Cochlea in the inner ear.
• Function: Convert sound vibrations into electrical signals for hearing.
• Regeneration: Very limited; damage often results in hearing loss.
6. Chondrocytes (in Articular Cartilage):
• Location: Cartilage in joints.
• Function: Maintain cartilage structure.
• Regeneration: Limited; damage can lead to joint degeneration and osteoarthritis.
Parenchymal epithelial cells are the functional cells of an organ that perform its primary functions. For example, in the liver, hepatocytes are parenchymal epithelial cells because they carry out the liver’s main functions, such as metabolism and detoxification. These cells are generally considered stable cells because they have a relatively slow rate of turnover and only divide when necessary (e.g., in response to injury).
Epithelial cells, on the other hand, are a broader category that includes all cells forming the epithelium, which covers body surfaces and lines organs and cavities. They can be classified as labile cells if they have a high turnover rate, constantly dividing to replace cells that are lost or damaged. Examples include cells in the skin’s epidermis and the lining of the gastrointestinal tract.
Key differences:
- Parenchymal Epithelial Cells: Functional cells of an organ, stable with slower turnover.
- Epithelial Cells: General category; can be labile (high turnover) or stable, depending on their specific location and function.
State two main ways the liver regenerate itself
Mechanism of regeneration of liver
• proliferation of remaining hepatocytes
• repopulation from progenitor cells(this one usually happens in cells or organs with many stem cells. Example is the bone marrow)
State two main ways the liver regenerate itself
Mechanism of regeneration of liver
• proliferation of remaining hepatocytes
• repopulation from progenitor cells(this one usually happens in cells or organs with many stem cells. Example is the bone marrow)
How does the liver regenerate itself using the progenitor cells pathway
Here is a step-by-step overview of how liver cells regenerate following tissue injury:
- Tissue Injury: Damage to liver tissue from factors like toxins, viruses, or physical injury disrupts hepatocytes and the surrounding extracellular matrix.
- Inflammatory Response: The injury triggers an inflammatory response where Kupffer cells (liver macrophages) and other immune cells are activated. These cells release cytokines and growth factors to initiate the repair process.
- Kupffer Cells: These macrophages in the liver sinusoids release pro-inflammatory cytokines like TNF (Tumor Necrosis Factor) and interleukin-6 (IL-6), which help orchestrate the regenerative response.
- Recruitment of Other Cells: Additional immune cells and cytokines are recruited to the injury site to clear dead cells and debris.
- Priming of Hepatocytes: Cytokines and growth factors (e.g., TNF, IL-6) prepare hepatocytes (liver cells) for proliferation. This involves the activation of intracellular signaling pathways that make hepatocytes responsive to growth factors.
- EGF and TGF-α: These growth factors are released and bind to the Epidermal Growth Factor Receptor (EGFR) on hepatocytes. This binding triggers signaling pathways that promote hepatocyte entry into the cell cycle. (TGF-beta is secreted by pericytes during angiogenesis. So alpha is in liver regeneration.)
- HGF: Hepatocyte Growth Factor binds to the MET receptor on hepatocytes, further stimulating cell proliferation and migration.
- Go to Gi Transition: Hepatocytes, which are normally in the quiescent G0 phase, re-enter the cell cycle. They transition from G0 to G1 phase, preparing to divide.
- Cell Cycle Progression: Hepatocytes progress through the cell cycle phases (G1, S, G2, M) where they replicate DNA and undergo mitosis to produce new cells.
- Division and Replication: Hepatocytes divide and replicate, resulting in an increase in the number of liver cells. This process helps replace damaged cells and restore liver function.
- Formation of New Liver Tissue: Newly formed hepatocytes integrate into the existing liver architecture, contributing to tissue repair.
- Degradation of Damaged ECM: Matrix metalloproteinases (MMPs) degrade damaged extracellular matrix components.
- Synthesis of New ECM: Fibroblasts and other cells produce new ECM components to support the newly proliferated hepatocytes and restore tissue structure.
- Reorganization of Hepatocytes: The regenerated hepatocytes reorganize to restore the liver’s structural integrity and functional capabilities.
- Normalization of Blood Flow: The sinusoidal blood flow is normalized as the new liver tissue integrates with the existing vascular network.
- Anti-inflammatory Response: The inflammatory response subsides, and anti-inflammatory cytokines are released to resolve inflammation and promote tissue healing.
- Restoration of Liver Function: The regenerated liver tissue begins to regain its normal functions, including detoxification, protein synthesis, and metabolic activities.
Liver regeneration involves an intricate process starting with an inflammatory response to injury, followed by priming of hepatocytes, activation of growth factors, and cell cycle re-entry. Hepatocytes proliferate and integrate into the liver tissue, supported by ECM remodeling. The process concludes with the resolution of inflammation and functional recovery of the liver.
How does the liver regenerate itself using the progenitor cells pathway
Here is a step-by-step overview of how liver cells regenerate following tissue injury:
- Tissue Injury: Damage to liver tissue from factors like toxins, viruses, or physical injury disrupts hepatocytes and the surrounding extracellular matrix.
- Inflammatory Response: The injury triggers an inflammatory response where Kupffer cells (liver macrophages) and other immune cells are activated. These cells release cytokines and growth factors to initiate the repair process.
- Kupffer Cells: These macrophages in the liver sinusoids release pro-inflammatory cytokines like TNF (Tumor Necrosis Factor) and interleukin-6 (IL-6), which help orchestrate the regenerative response.
- Recruitment of Other Cells: Additional immune cells and cytokines are recruited to the injury site to clear dead cells and debris.
- Priming of Hepatocytes: Cytokines and growth factors (e.g., TNF, IL-6) prepare hepatocytes (liver cells) for proliferation. This involves the activation of intracellular signaling pathways that make hepatocytes responsive to growth factors.
- EGF and TGF-α: These growth factors are released and bind to the Epidermal Growth Factor Receptor (EGFR) on hepatocytes. This binding triggers signaling pathways that promote hepatocyte entry into the cell cycle.
- HGF: Hepatocyte Growth Factor binds to the MET receptor on hepatocytes, further stimulating cell proliferation and migration. The primary ligand for the MET receptor is Hepatocyte Growth Factor (HGF), also known as Scatter Factor. Yes, the acronym MET stands for Mesenchymal-Epithelial Transition. In this context, the MET receptor (Hepatocyte Growth Factor Receptor)
- Go to Gi Transition: Hepatocytes, which are normally in the quiescent G0 phase, re-enter the cell cycle. They transition from G0 to G1 phase, preparing to divide.
- Cell Cycle Progression: Hepatocytes progress through the cell cycle phases (G1, S, G2, M) where they replicate DNA and undergo mitosis to produce new cells.
- Division and Replication: Hepatocytes divide and replicate, resulting in an increase in the number of liver cells. This process helps replace damaged cells and restore liver function.
- Formation of New Liver Tissue: Newly formed hepatocytes integrate into the existing liver architecture, contributing to tissue repair.
- Degradation of Damaged ECM: Matrix metalloproteinases (MMPs) degrade damaged extracellular matrix components.
- Synthesis of New ECM: Fibroblasts and other cells produce new ECM components to support the newly proliferated hepatocytes and restore tissue structure.
- Reorganization of Hepatocytes: The regenerated hepatocytes reorganize to restore the liver’s structural integrity and functional capabilities.
- Normalization of Blood Flow: The sinusoidal blood flow is normalized as the new liver tissue integrates with the existing vascular network.
- Anti-inflammatory Response: The inflammatory response subsides, and anti-inflammatory cytokines are released to resolve inflammation and promote tissue healing.
- Restoration of Liver Function: The regenerated liver tissue begins to regain its normal functions, including detoxification, protein synthesis, and metabolic activities.
Liver regeneration involves an intricate process starting with an inflammatory response to injury, followed by priming of hepatocytes, activation of growth factors, and cell cycle re-entry. Hepatocytes proliferate and integrate into the liver tissue, supported by ECM remodeling. The process concludes with the resolution of inflammation and functional recovery of the liver.
In liver regeneration, the process typically involves the following sequence:
- Initial Activation: Hepatocytes are initially in the quiescent G0 phase. In response to liver injury, they undergo a “priming” phase where they become responsive to growth factors. During this phase, cytokines and other signaling molecules are released, preparing the hepatocytes for cell cycle re-entry.
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Growth Factors: Growth factors such as HGF (Hepatocyte Growth Factor), EGF (Epidermal Growth Factor), and TGF-α (Transforming Growth Factor Alpha) are released and bind to their respective receptors on hepatocytes. For example:
- HGF binds to the MET receptor on hepatocytes.
- EGF and TGF-α bind to the Epidermal Growth Factor Receptor (EGFR) on hepatocytes.
- Receptor Activation: Binding of these growth factors to their receptors activates intracellular signaling pathways. This leads to the activation of cyclins and other cell cycle regulators.
- Entry into Cell Cycle: Once hepatocytes are primed and growth factor receptors are activated, hepatocytes transition from the G0 phase into the G1 phase of the cell cycle.
- Proliferation: During the G1 phase, the hepatocytes prepare for DNA replication and subsequent cell division. They progress through the cell cycle (G1, S, G2, M phases), leading to cell proliferation and tissue regeneration.
Hepatocytes first undergo priming in response to liver injury, becoming ready to enter the cell cycle. Growth factors then bind to their specific receptors on hepatocytes, activating signaling pathways that drive the hepatocytes to re-enter the cell cycle and proliferate. Thus, growth factors play a crucial role in stimulating hepatocytes to move from the quiescent G0 phase into active proliferation.
After mitosis, the hepatocytes go back into the G0 phase waiting for another stimulus to make them start the process all over again
You’re correct that IL-6 has an important role in priming hepatocytes to be more receptive to growth factors, which then drive the cells into the G1 phase. Here’s a more detailed breakdown:
- IL-6 Priming: IL-6 acts as a priming signal that prepares hepatocytes to respond to growth factors. When IL-6 is released, it activates various signaling pathways within the hepatocytes, which increases their responsiveness to growth factors like HGF and EGF.
- Transition to G1: After IL-6 primes the hepatocytes, they become more sensitive to the action of growth factors. These growth factors are then responsible for pushing the hepatocytes from the G0 phase (a quiescent state) into the G1 phase, marking the entry into the cell cycle.
So, while IL-6 itself doesn’t directly push cells into the G1 phase, it is crucial for making the cells receptive to the growth factors that do. Both IL-6 and growth factors are essential for the successful regeneration of liver tissue.
State three phases of tissue regeneration
-Priming- cells are in G0 phase and have to be sensitive to growth factors before they can be moved into G1 phase and undergo cell proliferation. IL-6 primes the cells to be sensitive to growth factors and growth factors cause the transition of the cells into to G1. IL-6 does not activate the growth factors themselves. Instead, it makes the hepatocytes more responsive to these growth factors
-Cell proliferation
-Termination
Which cells are always in the G0 phase until priming occurs?(stable or labile cells?)
In the context of stable and labile cells, the cells that are in the G0 phase until they are primed to move into the G1 phase are:
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Hepatocytes (Liver Cells):
- Location: Liver
- Function: Hepatocytes are in the G0 phase under normal conditions but can re-enter the cell cycle (G1 phase) in response to liver injury or regeneration signals.
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Renal Tubular Cells:
- Location: Kidneys
- Function: Renal tubular cells are typically in the G0 phase but can re-enter the cell cycle following kidney injury or stress.
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Pancreatic Cells:
- Location: Pancreas
- Function: Pancreatic cells, such as acinar cells, are in the G0 phase under normal conditions but can re-enter the cell cycle in response to damage or disease.
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Smooth Muscle Cells:
- Location: Blood vessels, intestines, and other organs
- Function: Smooth muscle cells are usually in the G0 phase but can re-enter the cell cycle in response to injury or pathological conditions.
- Note: Labile cells are constantly cycling through the cell cycle and are not typically in the G0 phase. They are continuously dividing and renewing, so they do not have a significant G0 phase.
Stable cells like hepatocytes, renal tubular cells, pancreatic cells, and smooth muscle cells remain in the G0 phase until they are stimulated by injury, disease, or other signals that prime them to enter the G1 phase and proceed through the cell cycle.
When does scar formation usually occur
Tissue repair - scar formation
“If repair cannot be accomplished by regeneration alone, it occurs by replacement of the injured cells with connective tissue, leading to the formation of a scar, or by a combination of regeneration of some residual cells and scar formation” true or false
What is the role of fibroblasts in repair?
What is the function of vascular endothelial cells in wound repair?
What is eschar
When inflammation is too much and the wound is too big so the cells can’t proliferate enough to close the wound entirely or bring the tissue back to its original architecture so it resorts to the deposition of collagen.
Collagen is mainly produced or secreted by cells in the connective tissue layer of the organ. These cells are called fibroblasts.
Vascular endothelial cells induce angiogenesis.s initially c the old epithelial tissue has access to the blood vessels but as the new one forms, the old one begins to detach itself. If you remove the eschar before it falls off or completely detached itself, you’ll see blood come because the eschar is still having access to the blood vessels and hasn’t completely detach et self.
The term eschar refers to a piece of dead tissue that is cast off from the surface of the skin, particularly after a burn, ulcer, or other forms of skin injury. Eschar is typically dark, dry, and hard, and it forms as part of the body’s natural healing process. Eschar is a scab-like layer of dead tissue that forms over a wound. As the underlying tissues heal, this layer eventually detaches, revealing new surface epithelium beneath.
While both eschar and scabs form protective layers over wounds, eschar is associated with more severe tissue damage and consists of dead tissue, whereas a scab is primarily formed from dried blood and wound exudates after superficial injuries.
