disease

ISCHEMIA

Entity Detail — Knowledge Graph Node

Understanding Entity Pages

This page aggregates everything SciDEX knows about ISCHEMIA: its mechanistic relationships (Knowledge Graph edges), hypotheses targeting it, analyses mentioning it, and supporting scientific papers. The interactive graph below shows its immediate neighbors. All content is AI-synthesized from peer-reviewed literature.

2593Connections

0Hypotheses

1Analyses

50Outgoing

50Incoming

0Experiments

1Debates

No summary available yet.

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Disease Info

Associated Genes	AKT, ALZHEIMER, AMPK, AMYLOID, amyotrophic lateral sclerosis, APP, BAX, BCL2
Therapeutic Agents	KAEMPFEROL
KG Connections	867 knowledge graph edges
Databases	OMIM Orphanet ClinicalTrials PubMed

Pathway Diagram

graph TD
    ISCHEMIA["ISCHEMIA"]
    LAMP1(["LAMP1"])
    ISCHEMIA -->|"regulates"| LAMP1
    MYC(["MYC"])
    ISCHEMIA -->|"regulates"| MYC
    RAS(["RAS"])
    ISCHEMIA -->|"regulates"| RAS
    SQSTM1(["SQSTM1"])
    ISCHEMIA -->|"activates"| SQSTM1
    NEURON["NEURON"]
    ISCHEMIA -->|"activates"| NEURON
    NEURONS["NEURONS"]
    ISCHEMIA -->|"activates"| NEURONS
    NEURODEGENERATION["NEURODEGENERATION"]
    NEURODEGENERATION -->|"associated_with"| ISCHEMIA
    APOPTOSIS["APOPTOSIS"]
    APOPTOSIS -->|"associated_with"| ISCHEMIA
    NEUROINFLAMMATION["NEUROINFLAMMATION"]
    NEUROINFLAMMATION -->|"associated_with"| ISCHEMIA
    AUTOPHAGY["AUTOPHAGY"]
    AUTOPHAGY -->|"associated_with"| ISCHEMIA
    style ISCHEMIA fill:#1a3a4a,stroke:#ef5350,stroke-width:3px,color:#e0e0e0

Outgoing (854)

Target	Relation	Type	Str
Neurodegeneration	activates	disease	1.00
Inflammation	regulates	disease	1.00
Cardiac	therapeutic_target	disease	1.00
Inflammation	activates	disease	1.00
Inflammation	therapeutic_target	disease	1.00
Cardiac	activates	disease	1.00
Oxidative Stress	regulates	pathway	1.00
Apoptosis	therapeutic_target	pathway	1.00
Apoptosis	inhibits	pathway	1.00
Autophagy	regulates	pathway	1.00
Angiogenesis	activates	pathway	1.00
Oxidative Stress	therapeutic_target	pathway	1.00
Oxidative Stress	inhibits	pathway	1.00
Apoptosis	activates	pathway	1.00
Inflammation	associated_with	disease	1.00
Autophagy	activates	pathway	1.00
Ferroptosis	activates	pathway	1.00
Oxidative Stress	activates	pathway	1.00
Mitophagy	regulates	pathway	1.00
Apoptosis	regulates	pathway	1.00
Inflammation	treats	disease	0.95
Autophagy	upregulates	process	0.95
Alzheimer	associated_with	disease	0.95
Inflammation	inhibits	disease	0.95
AUTOPHAGY	upregulates	process	0.95
ALOX12	upregulates	gene	0.90
Lipid Droplet Accumulation	promotes	phenotype	0.90
Ferroptosis	therapeutic_target	pathway	0.90
Ferroptosis	inhibits	pathway	0.90
Autophagy	therapeutic_target	pathway	0.90
Immune Response	activates	pathway	0.90
Pi3K/Akt	activates	pathway	0.85
Myocardial Infarction	activates	disease	0.85
Neurodegeneration	regulates	disease	0.85
TNF-α	upregulates	protein	0.85
Myocardial Infarction	therapeutic_target	disease	0.85
IL-6	upregulates	protein	0.85
Cardiac	associated_with	disease	0.85
Apoptosis	causes	pathway	0.85
IL-1β	upregulates	protein	0.85
Neurodegeneration	associated_with	disease	0.85
NEURODEGENERATION	contributes_to	process	0.80
MACROPHAGES	activates	cell_type	0.80
NLRP3	activates	protein	0.80
Blood-Brain Barrier	therapeutic_target	pathway	0.80
Mitochondrial Function	activates	pathway	0.80
Apoptosis	associated_with	pathway	0.80
Mitophagy	associated_with	pathway	0.80
Oxidative Stress	associated_with	pathway	0.80
Stem Cell	activates	pathway	0.80

Incoming (1739)

Source	Relation	Type	Str
MITOCHONDRIA	therapeutic_target	gene	1.00
INFLAMMATION	activates	gene	1.00
MITOPHAGY	regulates	gene	1.00
Als	activates	disease	1.00
AKT	activates	gene	1.00
Stroke	inhibits	disease	1.00
APOPTOSIS	regulates	gene	1.00
OXIDATIVE STRESS	regulates	gene	1.00
APOPTOSIS	inhibits	gene	1.00
INFLAMMATION	regulates	gene	1.00
APOPTOSIS	therapeutic_target	gene	1.00
ALZHEIMER'S DISEASE	associated_with	disease	1.00
AUTOPHAGY	activates	gene	1.00
AUTOPHAGY	regulates	gene	1.00
INFLAMMATION	inhibits	gene	1.00
APOPTOSIS	activates	gene	1.00
OXIDATIVE STRESS	activates	gene	1.00
Stroke	therapeutic_target	disease	1.00
NEURODEGENERATION	regulates	gene	1.00
ALZHEIMER'S DISEASE	associated_with	gene	1.00
ASTROCYTES	associated_with	cell_type	1.00
STROKE	inhibits	gene	1.00
ASTROCYTES	activates	gene	1.00
Als	regulates	disease	1.00
NEURODEGENERATION	activates	gene	1.00
MICROGLIA	associated_with	cell_type	1.00
FERROPTOSIS	activates	gene	1.00
OXIDATIVE STRESS	inhibits	gene	1.00
GENES	activates	gene	1.00
Stroke	activates	disease	1.00
Als	associated_with	disease	1.00
Als	therapeutic_target	disease	1.00
ROS	activates	gene	1.00
Cardiovascular	therapeutic_target	disease	1.00
STROKE	associated_with	gene	1.00
ALZHEIMER	associated_with	gene	1.00
STROKE	therapeutic_target	gene	1.00
PARKINSON	associated_with	gene	1.00
STROKE	activates	gene	1.00
INFLAMMATION	therapeutic_target	gene	1.00
OXIDATIVE STRESS	therapeutic_target	gene	1.00
VEGF	activates	gene	1.00
MITOCHONDRIA	activates	gene	1.00
MICROGLIA	regulates	gene	1.00
IL-6	inhibits	gene	0.95
APOPTOSIS	causes	gene	0.95
TNF	activates	gene	0.95
FERROPTOSIS	therapeutic_target	gene	0.95
Als	inhibits	disease	0.95
INFLAMMATION	treats	gene	0.95

Targeting Hypotheses (0)

Hypotheses where this entity is a therapeutic target

Hypothesis	Score	Disease	Analysis
No targeting hypotheses

Mentioning Analyses (1)

Scientific analyses that reference this entity

Does TFEB dysfunction cause neurodegeneration or represent a compensatory respon

neurodegeneration | 2026-04-03 | 7 hypotheses Top: 0.697

Experiments (0)

Experimental studies targeting or related to this entity

Experiment	Type	Disease	Score	Feasibility	Model	Status	Est. Cost
No experiments found

Related Papers (0)

Scientific publications cited in analyses involving this entity

Title & PMID	Authors	Journal	Year	Citations
No papers found

Debates (1)

Multi-agent debates referencing this entity

The debate highlighted TFEB's role in mitochondrial-lysosomal coupling but could

closed · Rounds: 4 · Score: 0.95 · 2026-04-03

Related Research

Hypotheses and analyses mentioning ISCHEMIA in their description or question text

No additional research found