cell final Flashcards

lec 20-27

1
Q

what does cell division refer to

A

the creation of two daughter cells from one parent cell

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2
Q

what are daughter cells identical to

A

each other and to the parent cell

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3
Q

why is cell division tightly regulated

A

to prevent the overproduction of cells

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4
Q

what does the term cell cycle refer to

A

a series of stages that a cell progresses through before cell division can occur

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5
Q

what are the 4 sequential stages of cell division

A

G1, S, G2, M

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6
Q

what does the G2 phase do

A

prepare the cell for DNA replication

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7
Q

what happens during the G1 phase

A

The cell grows, makes mRNA and proteins for DNA replication, and produces energy. It commits to the cell cycle at the START point.

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8
Q

what is START

A

a process where the cell is committed to progress through the remainder of the cell cycle

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9
Q

what happens during the S phase

A

the parent cell’s DNA is replicated

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10
Q

what are sister chromatids held together by

A

cohesions

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11
Q

what is a centromere

A

the region where the
kinetochore will form and microtubules will bind

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12
Q

what is a centrosome

A

a microtubule organizing center

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13
Q

what happens during the G2 phase

A

The cell checks for DNA replication errors, finishes centrosome duplication, and starts forming microtubules for mitosis.

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14
Q

What are the stages of mitosis and their functions?

A

Prophase: Chromosomes condense, nuclear envelope breaks, spindle forms.
Metaphase: Chromosomes align at the center.
Anaphase: Cohesins are degraded, and chromatids are pulled apart.
Telophase: Chromosomes decondense, nuclear envelope reforms.

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15
Q

What causes the chromosome number to double during anaphase?

A

Sister chromatids are separated into individual chromosomes.

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16
Q

What cells enter G0 permanently?

A

ostmitotic cells like neurons

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17
Q

Can any cells leave G0 and re-enter the cycle?

A

Yes, some dividing cells temporarily enter G0 and can rejoin the cycle later.

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18
Q

what is the difference between G1 and Go phases

A

G1 is part of the cycle where the cell grows and prepares to replicate DNA. G0 is a resting phase where cells exit the cycle and do not divide (often permanently).

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19
Q

What two proteins form the complex that regulates the cell cycle?

A

Cyclin (regulatory subunit) and CDK (cyclin-dependent kinase, catalytic subunit).

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20
Q

How does cyclin control CDK?

A

It activates CDK and determines which proteins it can phosphorylate.

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21
Q

How is cyclin level regulated?

A

Through transcriptional waves (increased production) and proteasomal degradation (breakdown after phase completion).

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22
Q

What are mitogens and anti-mitogens?

A

Mitogens promote G1 entry by increasing cyclin/CDK levels. Anti-mitogens do the opposite and inhibit entry.

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23
Q

What enzymes regulate CDK through phosphorylation?

A

CAK (CDK-activating kinase): Activates CDK
Wee1 kinase: Inhibits CDK
CDK inhibitors: Bind to and block cyclin-CDK complexes

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24
Q

What triggers the transition from G2 to M phase?

A

Dephosphorylation of CDK (by inactivating Wee1 and activating phosphatases).

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25
Q

How is the cycle reset after mitosis?

A

M phase cyclins are degraded, CDK inhibitors are produced, and CDK targets are dephosphorylated.

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26
Q

What are the components of a checkpoint pathway?

A

A sensor (detects error), signaling cascade (alerts the cell), and effector (halts the cycle and activates repair).

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27
Q

What happens if DNA damage is detected?

A

CDKs are inactivated, the cell cycle is halted, and repair is attempted. If damage is unfixable, the cell undergoes apoptosis

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28
Q

What does the spindle assembly checkpoint do?

A

It ensures all chromosomes are attached to spindle fibers before anaphase, preventing chromosome mis-segregation.

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29
Q

How do cells contribute to tissue and organ formation?

A

Cells of the same type aggregate to form tissues, tissues combine to make organs, and organs associate to form organ systems.

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30
Q

Give an example of this organizational hierarchy.

A

Myocytes form muscle fascicles → fascicles combine with other tissues to form skeletal muscle → skeletal muscles associate with bones to form the musculoskeletal system.

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31
Q

What is a key hallmark of metastatic tumors?

A

The breakdown of cell-cell adhesion.

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32
Q

Why is cell adhesion important in multicellular organisms?

A

It allows cells to associate with one another and the extracellular environment, which is essential for tissue structure and function.

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33
Q

What mediates cell-cell adhesion?

A

Cell-adhesion molecules (CAMs) on the plasma membrane.

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34
Q

What mediates cell-matrix adhesion?

A

Adhesion receptors such as integrins that bind to extracellular matrix proteins.

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35
Q

What are CAMs and what do they do?

A

CAMs are membrane proteins that extend into the extracellular space and bind to other CAMs (same or different) on neighboring cells.

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36
Q

How are CAMs linked internally in the cell?

A

They are connected to the cytoskeleton and can initiate intracellular signaling.

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37
Q

Where do CAMs cluster?

A

In structures called cell junctions.

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38
Q

What are the three major types of cell junctions?

A

Tight junctions
Anchoring junctions
Gap junctions

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39
Q

What is the function of tight junctions?

A

They form a seal that prevents molecules from passing between cells (paracellular pathway), forcing substances to go through cells instead (transcellular pathway).

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40
Q

What proteins make up tight junctions?

A

Occludin, claudin, and junction adhesion molecules (JAMs).

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41
Q

What do anchoring junctions do?

A

They create stable links between cells and their cytoskeletons, providing structural support and allowing force transmission.

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42
Q

What are the two types of anchoring junctions?

A

Adherens junctions: Act like zippers
Desmosomes: Act like spot welds

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43
Q

What is the function of gap junctions?

A

They allow direct passage of ions and small molecules (like second messengers) between neighboring cells.

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44
Q

What proteins form gap junctions?

A

Connexins — 6 from each cell align to form a continuous channel.

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45
Q

What is the ECM composed of?

A

Proteoglycans: Form gel-like substances that resist compression
Collagen: Provides strength and structure
Multi-adhesive matrix proteins: Help organize and stabilize ECM (e.g., laminin)

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46
Q

What are integrins and what do they bind to?

A

Integrins are transmembrane receptors that bind to ECM components like collagen, laminin, and fibronectin.

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47
Q

How strong are integrin interactions, and how is strength achieved?

A

Individually weak, but strong when many integrins cluster together at junctions.

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48
Q

What are focal adhesions?

A

Junctions that connect ECM proteins to cytosolic microfilaments.

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49
Q

What are hemidesmosomes?

A

Junctions that connect ECM proteins to intermediate filaments inside the cell.

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50
Q

What are stem cells?

A

Unspecialized cells that can differentiate into other cell types and self-renew to maintain their population.

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51
Q

What is self-renewal?

A

The ability of stem cells to divide and produce more stem cells throughout an organism’s life.

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52
Q

What are pluripotent stem cells?

A

Stem cells that can become any cell type in the body (e.g., embryonic stem cells).

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53
Q

What are multipotent stem cells?

A

Stem cells that can differentiate into several, but not all, specialized cell types (e.g., hematopoietic stem cells in adults).

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54
Q

What is asymmetric division in stem cells?

A

A type of division where one daughter cell remains a stem cell and the other becomes a differentiated cell.

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55
Q

What triggers asymmetric division?

A

Polarity signals—signaling molecules on one side of the cell lead to reorganization of the cell’s contents before division.

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56
Q

What is symmetric division in stem cells?

A

A division where both daughter cells either remain stem cells or both become differentiated cells.

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57
Q

What is a stem cell niche?

A

The environment containing signals required for stem cell maintenance, division, and differentiation.

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58
Q

What happens when stem cells are removed from their niche?

A

They may lose some of their stem cell properties.

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59
Q

What are intrinsic regulatory signals in stem cells?

A

Internal mechanisms that help maintain stem cell identity and behavior.

60
Q

What are extrinsic signals?

A

External cues (like signaling molecules) from the niche that influence stem cell division and differentiation.

61
Q

What are progenitor cells?

A

Cells that are partially differentiated, have limited self-renewal, and can only become one or a few cell types.

62
Q

How are progenitor cells related to stem cells?

A

Many stem cells first become progenitor cells before becoming fully differentiated.

63
Q

What are iPS cells?

A

Differentiated cells that are reprogrammed to become pluripotent stem cells using synthetic biology.

64
Q

What is the source of all blood and immune cells?

A

Hematopoietic stem cells.

65
Q

What is the role of Notch signaling in stem cells?

A

It regulates stem cell fate decisions and homeostasis.

66
Q

How does Notch signaling influence cell outcomes?

A

High Notch activity pushes cells toward differentiation; low Notch activity maintains stem cell identity.

67
Q

What is optogenetics used for in stem cell research?

A

To control and study cell fate decisions by manipulating light-sensitive signaling pathways during division

68
Q

What are the two main types of cell death?

A

Necrosis and apoptosis

69
Q

What distinguishes necrosis from apoptosis?

A

Necrosis is a passive form of cell death caused by injury, releasing cell contents and inducing inflammation. Apoptosis is a programmed process that avoids inflammation by packaging cell contents into fragments that are phagocytosed.

70
Q

Name two environmental factors that can affect cell lifespan.

A

Infections and toxic substances

71
Q

What endogenous molecules influence a cell’s survival or death?

A

Trophic factors promote survival, while other endogenous signals stimulate cell death.

72
Q

What family of enzymes is central to apoptosis?

73
Q

How are caspases activated?

A

They are synthesized as inactive procaspases and activated by proteolytic cleavage.

74
Q

What is the difference between initiator and effector caspases?

A

Initiator caspases activate other caspases, while effector caspases cleave cellular proteins to carry out apoptosis.

75
Q

What triggers the extrinsic pathway of apoptosis?

A

External signaling molecules bind to death receptors on the plasma membrane.

76
Q

Which caspases are involved in the extrinsic pathway?

A

Caspase 8 (initiator) and caspase 3 (effector).

77
Q

What triggers the intrinsic pathway of apoptosis?

A

Internal cell stress such as infections, radiation, or hypoxia causing mitochondrial damage.

78
Q

What mitochondrial protein is released during the intrinsic pathway?

A

Cytochrome c.

79
Q

Which caspases are involved in the intrinsic pathway?

A

Caspase 9 (initiator) and caspase 3 (effector).

80
Q

What are the two main components of the immune system?

A

The innate immune system and the adaptive immune system

81
Q

What are the general functions of the immune system?

A

To protect the body from invading microorganisms and promote tissue repair.

82
Q

What are examples of physical barriers in the human body?

A

Skin and mucous membranes lining the gastrointestinal, genitourinary, and respiratory tracts.

83
Q

What are the characteristics of the innate immune system?

A

Rapid, non-specific response that acts within minutes. It recognizes common microbial features and contains the infection until the adaptive immune system is activated.

84
Q

How do chemical barriers protect against microbes?

A

Substances like sweat, tears, and saliva contain antimicrobial enzymes such as defensins. Mucus and earwax trap microbes and limit access to epithelial cells.

85
Q

Which cells are part of the innate immune system?

A

Monocytes, macrophages, neutrophils, eosinophils, basophils, mast cells, and dendritic cells.

86
Q

What is the function of monocytes and how do they change in tissues?

A

Monocytes circulate in the bloodstream and differentiate into macrophages once they enter tissues.

87
Q

What are the roles of macrophages?

A

Detect and engulf pathogens (phagocytosis), destroy them with enzymes, release cytokines and chemokines, and present antigens to T cells using MHC Class II.

88
Q

What is the role of neutrophils?

A

They are the most abundant white blood cells, engulf pathogens through phagocytosis, and release cytokines.

89
Q

What immune roles do eosinophils, basophils, and mast cells play?

A

Eosinophils are involved in allergic reactions and parasitic defense; basophils and mast cells release inflammatory mediators.

90
Q

What is a dendritic cell’s main function?

A

Acts as a professional antigen-presenting cell, migrating to lymph nodes to activate adaptive immune cells and secreting cytokines to guide immune responses.

91
Q

What are the defining features of the adaptive immune system?

A

Specific and delayed response (4–7 days after infection), involving B cells and T cells that recognize specific antigens.

92
Q

What is an epitope?

A

A specific region of an antigen to which an antibody binds.

93
Q

What are memory cells and what is their function?

A

Subsets of adaptive immune cells that provide long-term immunity by responding more effectively upon re-exposure to the same pathogen.

94
Q

What are the two main types of adaptive immunity?

A

active immunity, which includes natural immunity and artificially acquired immunity. The second type of adaptive immunity is called passive immunity

95
Q

What two antagonistic processes regulate cell numbers in tissues?

A

Proliferation and cell death.

96
Q

What promotes cell proliferation, and what promotes cell death?

A

Mitogens and growth factors promote proliferation; absence of survival signals promotes cell death.

97
Q

What is a tumor?

A

A tumor is an abnormal growth of cells that serves no functional purpose in the body.

98
Q

What is the difference between benign and malignant tumors?

A

Benign tumors: Non-cancerous, well-differentiated, do not invade surrounding tissue.
Malignant tumors: Cancerous, less differentiated, proliferate rapidly, can invade other tissues (metastasize).

99
Q

Do all cells in the body proliferate throughout life?

A

No. For example, epithelial cells proliferate continuously, while neurons are terminally differentiated and do not divide.

100
Q

How is apoptosis involved in preventing cancer?

A

It eliminates damaged or genetically unstable cells before they can proliferate abnormally.

101
Q

What are the two main classes of genes mutated in cancer?

A

Proto-oncogenes and tumor suppressor genes.

102
Q

How do proto-oncogenes contribute to cancer when mutated

A

They become oncogenes, which drive increased cell proliferation. Example: Ras.

103
Q

What happens when tumor suppressor genes are inhibited?

A

Apoptosis is reduced and uncontrolled cell proliferation occurs. Example: p53.

104
Q

What are five key characteristics of cancer cells?

A
  1. Enhanced proliferation (even without growth signals)
  2. Resistance to apoptosis
  3. Less differentiation
  4. Induce blood vessel formation (angiogenesis)
  5. Increased mobility and invasiveness
105
Q

What is metastasis?

A

The process by which cancer cells spread from their site of origin to other parts of the body.

106
Q

What steps are required for metastasis to occur?

A
  1. Break cell-cell and cell-matrix adhesions
  2. Migrate through tissue
  3. Degrade extracellular matrix proteins
  4. Enter bloodstream
  5. Travel and survive in new tissue
107
Q

What increases an individual’s risk of developing cancer?

A

Exposure to carcinogens

108
Q

What are carcinogens?

A

Substances or exposures that can lead to cancer by causing mutations in DNA.

109
Q

What is the difference between proto-oncogenes and oncogenes?

A

Proto-oncogenes are normal genes that regulate cell growth. When mutated, they
become oncogenes, which can cause uncontrolled cell proliferation.

110
Q

What is a classical example of a proto-oncogene?

111
Q

What happens when tumor suppressor genes are inhibited?

A

Inhibition of tumor suppressor genes reduces apoptosis and increases cell proliferation,
potentially leading to cancer.

112
Q

What is a classical example of a tumor suppressor gene?

113
Q

What is Simian Virus 40 (SV40)?

A

SV40 is an oncogenic virus that has been associated with cancer development.

114
Q

What receptor does SV40 use to enter host cells?

A

Ganglioside receptor GM1.

115
Q

Who was Alton Ochsner and what incident is associated with him?

A

Alton Ochsner was involved in an incident where he injected his grandchildren with a
tainted polio vaccine, resulting in the death of his grandson and polio in his granddaughter.

116
Q

What role did Bernice Eddy play in the context of SV40?

A

Bernice Eddy discovered the contamination of polio vaccines with SV40.

117
Q

What does the SV40 genome map show?

A

It illustrates the organization of viral genes and regulatory elements within SV40.

118
Q

What are the cellular targets of SV40 during infection?

A

SV40 targets regulatory pathways controlling cell proliferation and apoptosis.

119
Q

What are the two main classes of genes mutated during cancer development?

A

Proto-oncogenes (become oncogenes) and tumor suppressor genes.

120
Q

How can viruses induce tumorigenesis through cellular fusion?

A

Viral infection can cause fusion of infected cells with healthy ones, potentially leading to
uncontrolled cell growth.

121
Q

What is cellular senescence?

A

A state in which cells permanently stop dividing but do not die, often acting as a natural
barrier to cancer.

122
Q

What is the role of Ras in cancer development?

A

Ras is a proto-oncogene that, when mutated, becomes an oncogene that promotes
uncontrolled cell proliferation.

123
Q

How does the loss of p53 contribute to tumor formation?

A

p53 is a tumor suppressor gene that promotes apoptosis; its loss prevents damaged cells
from dying, leading to unchecked cell growth.

124
Q

What is the significance of SV40’s interaction with host cell machinery?

A

SV40 can hijack host cell machinery to replicate and interfere with normal cell cycle
regulation, contributing to cancer development.

125
Q

What was the Cutter incident?

A

A mishap in which a batch of polio vaccine contaminated with SV40 from Cutter
Laboratories caused illness and death.

126
Q

What type of virus is SV40 and how does it package its DNA?

A

SV40 is a DNA virus that tightly packs its circular DNA genome using host histones,
resembling mini-chromosomes.

127
Q

What is cellular senescence?

A

A state of stable cell cycle arrest in which cells become resistant to growth-promoting
stimuli, often due to DNA damage.

128
Q

Who first described cellular senescence?

A

Leonard Hayflick, through his studies on human fetal fibroblasts.

129
Q

What are key features of senescent cells?

A

Morphological and metabolic changes, chromatin reorganization, altered gene
expression, and SASP.

130
Q

What does SASP stand for?

A

Senescence-Associated Secretory Phenotype.

131
Q

How can senescent cells be detected histologically?

A

By β-Galactosidase staining at pH 6.0, which turns cells blue.

132
Q

What DNA marker is commonly used for senescence?

A

Histone2A.X, which marks DNA damage sites.

133
Q

What is the role of p53 in senescence?

A

It is activated in response to cellular stress and DNA damage, promoting cell cycle arrest.

134
Q

How does senescence help prevent cancer?

A

By stopping replication of cells with damaged DNA

135
Q

What unintended effect can chemotherapy have related to senescence?

A

It can induce senescence in normal cells, leading to fatigue and other side effects.

136
Q

How do senescent cells contribute to aging?

A

They accumulate over time and are associated with tissue degeneration and
inflammation.

137
Q

Are aging and senescence the same?

A

No, aging is a time-based decline, while senescence occurs throughout life, even during
development.

138
Q

How do telomeres relate to senescence?

A

Telomeres shorten with each division; once critically short, they trigger senescence.

139
Q

What is the “end replication problem”?

A

DNA polymerase cannot fully replicate the ends of the lagging strand, causing telomere
shortening

140
Q

Which enzyme prevents telomere shortening in cancer cells?

A

Telomerase

141
Q

What happens when telomeres reach a critical length?

A

They are recognized as DNA damage, leading to cell cycle arrest.

142
Q

What are senolytics?

A

Therapeutic agents that selectively eliminate senescent cells.

143
Q

What are potential benefits of senolytics in animal models?

A

Reduced inflammation, better immune function, and slowed age-related disease.

144
Q

Name three senolytic compounds mentioned in the research.

A

Dasatinib, Quercetin, and Fisetin.

145
Q

What age-related diseases are senolytics being tested for in humans?

A

Osteoarthritis and chronic kidney disease.

146
Q

How might senolytics affect lifespan?

A

They can extend lifespan and reduce physical decline in aging models.