MindMap Gallery Cell Biology-Cell Aging and Death Mind Map
This is a mind map about cell biology - cell aging and death. As time goes by, the proliferation ability and physiological functions of cells gradually decline, leading to irreversible growth stagnation, which ultimately leads to the death of C.
Edited at 2023-12-02 16:31:22El cáncer de pulmón es un tumor maligno que se origina en la mucosa bronquial o las glándulas de los pulmones. Es uno de los tumores malignos con mayor morbilidad y mortalidad y mayor amenaza para la salud y la vida humana.
La diabetes es una enfermedad crónica con hiperglucemia como signo principal. Es causada principalmente por una disminución en la secreción de insulina causada por una disfunción de las células de los islotes pancreáticos, o porque el cuerpo es insensible a la acción de la insulina (es decir, resistencia a la insulina), o ambas cosas. la glucosa en la sangre es ineficaz para ser utilizada y almacenada.
El sistema digestivo es uno de los nueve sistemas principales del cuerpo humano y es el principal responsable de la ingesta, digestión, absorción y excreción de los alimentos. Consta de dos partes principales: el tracto digestivo y las glándulas digestivas.
El cáncer de pulmón es un tumor maligno que se origina en la mucosa bronquial o las glándulas de los pulmones. Es uno de los tumores malignos con mayor morbilidad y mortalidad y mayor amenaza para la salud y la vida humana.
La diabetes es una enfermedad crónica con hiperglucemia como signo principal. Es causada principalmente por una disminución en la secreción de insulina causada por una disfunción de las células de los islotes pancreáticos, o porque el cuerpo es insensible a la acción de la insulina (es decir, resistencia a la insulina), o ambas cosas. la glucosa en la sangre es ineficaz para ser utilizada y almacenada.
El sistema digestivo es uno de los nueve sistemas principales del cuerpo humano y es el principal responsable de la ingesta, digestión, absorción y excreción de los alimentos. Consta de dos partes principales: el tracto digestivo y las glándulas digestivas.
Cellular senescence and death
1. Cellular senescence
As time goes by, the cell's proliferation ability and physiological functions gradually undergo a process of decline, leading to irreversible growth stagnation, which ultimately leads to the death of C
1. Cell senescence theory
①The theory of genetic determination
Progeria in infants and young children, autosomal recessive, mutation in the gene encoding nuclear membrane protein
In premature aging in adults, DNA cannot be repaired normally.
②Free radical theory: Reactive oxygen groups cause cell damage and aging
③Telomere theory
2.Characteristics of cell senescence
① Cell aging and body aging are both different and related
②The lifespan of various types of cells in the body is different
Approaching lifespan: N cells, fat cells, muscle cells
Slow renewal: liver cells, gastric parietal cells
Fast update: skin epidermal cells, red blood cells, white blood cells
③Life span of cells under in vitro culture conditions
3. Manifestations of cellular senescence
① Morphological changes: plasma membrane, cytoplasm, mitochondria, Golgi apparatus, inclusions, nucleus, nuclear membrane, chromatin, Nissl bodies
② Metabolic changes of biological macromolecules: DNA, RNA, proteins, enzyme molecules, lipids
4. Aging mechanism
The G1-S phase is an important restriction control point. It is the only control point where proliferating cells can receive external proliferation and inhibition information.
① Regulation of cellular replicative senescence: DNA damage caused by shortening of telomere ends activates p53 and promotes the transduction and translation of p21. p21 inhibits the cyclin-Cdk2 complex and inhibits the transition from G1 to S phase.
② Oxidative stress-induced telomere-independent cellular senescence, ERK, MAPK pathways, P16 inhibits Rb phosphorylation
2. Cell death
2. Morphological changes of apoptosis
① Changes in the nucleus: Nuclear DNA fragments into nucleosome fragments at nucleosome junctions, and the heterochromatin deaggregates and condenses into chromatin blocks under the nuclear membrane or in the central part.
② Cytoplasmic changes: significant concentration occurs, organelles change, and the cytoskeleton becomes dense and disordered
③Changes in the cell membrane: The specialized structure disappears, but the cell membrane remains intact and has selective permeability.
④Formation of apoptotic bodies
(a) Germination and shedding mechanism: formation of membrane inclusions and apoptotic bodies of varying sizes containing cytoplasm, organelles, and nuclear fragments
(b) Segmentation mechanism: ER is divided into compartments of different sizes. The compartment membrane near the end of the cell membrane fuses with the cell membrane and falls off to form apoptotic bodies.
(c) Autophagosome formation mechanism: Organelles such as the mitochondrial endoplasmic reticulum and other cytoplasmic components are wrapped by the endoplasmic reticulum membrane to form autophagosomes, which fuse with the apoptotic C membrane and are excreted out of the cell to form apoptotic bodies.
3. Metabolic changes of macromolecules and C organs
①DNA fragmentation: endogenous endonuclease is activated
②C Protease in apoptosis
③Changes in cytoplasmic calcium ions and pH
④ Mitochondria: Respiratory chain is damaged; cytochrome C is released; ROS increases; osmotic transition pore permeability increases
4.Influencing factors
①Causing factors
(a) Physiological induction factors: tumor necrosis factor and its Fas ligand, calcium ions, glucocorticoids
(b) Damage-related factors
(c) Treatment-related factors: radiotherapy and chemotherapy
(d) Certain cytotoxic substances
②Inhibitory factors
(a) Physiological inhibitory factors: bcl-2 proto-oncogene, mutant p53
(b) Viral genes; promote infection and replication
(c) Others
5. Molecular mechanism
Inhibits: p53, ICE, FAS/FASL gene family
Promote or inhibit: Ced, Bcl-2, c-myc gene family
6.Detection
①Morphological detection
②Biochemical characteristics detection: gel electrophoresis
③Flow cytometer: changes in light scattering characteristics
3. Autophagy
The biological process of massive degradation of intracytoplasmic macromolecules and organelles in membrane vesicles
1. Classification: microautophagy, macroautophagy (most), molecular chaperone-mediated autophagy (no vesicles required)
2. Occurrence process: Substrate-induced formation of autophagy precursors, formation of autophagosomes, fusion of autophagosomes and lysosomes, and degradation of autophagosome contents
3. Regulation of autophagy: type III PI3K, mTOR signaling pathway, tumor suppressor PTEN, p53