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Related Concept Videos

Complement System01:27

Complement System

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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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Cellular Injury I: Introduction01:00

Cellular Injury I: Introduction

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Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
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Cellular Injury IlI: Cellular Death01:11

Cellular Injury IlI: Cellular Death

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Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...
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Cellular Injury II: Classification01:21

Cellular Injury II: Classification

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Cellular injury is any process that disrupts a cell’s ability to maintain homeostasis, leading to structural or functional changes. It is broadly classified based on etiology (cause) and mechanism of damage.Classification by EtiologyCellular injury may result from several causes. Hypoxic injury happens due to reduced oxygen delivery, most commonly from inadequate blood supply, such as arterial obstruction; for example, coronary artery thrombosis can cause myocardial infarction. Chemical...
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Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

221
Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...
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Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

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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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In Vitro Methods for Comparing Target Binding and CDC Induction Between Therapeutic Antibodies: Applications in Biosimilarity Analysis
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Complement-mediated cellular injury.

Tomoko Takano1, Hanan Elimam, Andrey V Cybulsky

  • 1Department of Medicine, McGill University Health Centre, McGill University, Montreal, Quebec, Canada.

Seminars in Nephrology
|October 29, 2013
PubMed
Summary
This summary is machine-generated.

The complement system

Keywords:
C5b-9 membrane attack complexcytoskeletonglomerulonephritisphospholipasesprotein kinases

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Depletion of Specific Cell Populations by Complement Depletion
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Depletion of Specific Cell Populations by Complement Depletion
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Area of Science:

  • Immunology
  • Nephrology
  • Cell Biology

Background:

  • Complement activation is crucial for bacterial defense but can cause cellular injury.
  • The C5b-9 membrane attack complex (MAC) contributes to kidney disease pathogenesis.
  • Sublytic MAC affects podocytes and other kidney cells, impacting cellular pathways and structures.

Purpose of the Study:

  • To elucidate the role of the terminal complement pathway in kidney cell injury.
  • To investigate the mechanisms by which C5b-9 induces damage in various kidney cell types.
  • To understand both injurious and protective roles of complement in kidney pathology.

Main Methods:

  • Utilized experimental models, including rat passive Heymann nephritis.
  • Investigated downstream signaling pathways activated by sublytic C5b-9 in podocytes.
  • Examined the effects of C5b-9 on mesangial, glomerular endothelial, and tubular epithelial cells.

Main Results:

  • Sublytic C5b-9 activates diverse pathways in podocytes, affecting protein kinases, lipid metabolism, and cellular integrity.
  • C5b-9 causes injury to multiple kidney cell types, contributing to glomerulonephritis, thrombotic microangiopathy, and acute kidney injury.
  • Complement cleavage products like C5a and C1q also demonstrate kidney cell toxicity.

Conclusions:

  • The terminal complement pathway, particularly C5b-9, plays a significant role in kidney cell injury and disease.
  • Complement-mediated kidney damage occurs through both inflammation-dependent and independent mechanisms.
  • Understanding complement's dual role is vital for developing therapeutic strategies for kidney diseases.