PLIN5 — Perilipin 5

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PLIN5 — Perilipin 5

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PLIN5 — Perilipin 5

Overview

<table class="infobox infobox-gene">
<tr>
<th class="infobox-header" colspan="2">PLIN5 — Perilipin 5</th>
</tr>
<tr>
<td class="label">Gene Symbol</td>
<td>PLIN5</td>
</tr>
<tr>
<td class="label">Gene Name</td>
<td>Perilipin 5 (OXPAT)</td>
</tr>
<tr>
<td class="label">Chromosomal Location</td>
<td>9q34.3</td>
</tr>
<tr>
<td class="label">NCBI Gene ID</td>
<td>440503</td>
</tr>
<tr>
<td class="label">Ensembl ID</td>
<td>ENSG00000165030</td>
</tr>
<tr>
<td class="label">OMIM ID</td>
<td>613877</td>
</tr>
<tr>
<td class="label">UniProt ID</td>
<td>Q0VGN5 (PLIN5_HUMAN)</td>
</tr>
<tr>
<td class="label">Total Exons</td>
<td>7</td>
</tr>
<tr>
<td class="label">Transcript Length</td>
<td>~1,500 bp (coding sequence)</td>
</tr>
<tr>
<td class="label">Protein Length</td>
<td>463 amino acids</td>
</tr>
<tr>
<td class="label">Protein Mass</td>
<td>~50 kDa</td>
</tr>
<tr>
<td class="label">Expression Priority Tissues</td>
<td>Heart, skeletal muscle, brown adipose tissue, brain (neurons, astrocytes, microglia)</td>
</tr>
<tr>
<td class="label">Family</td>
<td>Perilipin family (PLIN1-5)</td>
</tr>
<tr>
<td class="label">Modes of Inheritance</td>
<td>Complex inheritance (metabolic traits); rare monogenic forms</td>
</tr>
<tr>
<td class="label">Tissue</td>
<td>Expression Level</td>
</tr>
<tr>
<td class="label">

...

PLIN5 — Perilipin 5

Overview

<table class="infobox infobox-gene">
<tr>
<th class="infobox-header" colspan="2">PLIN5 — Perilipin 5</th>
</tr>
<tr>
<td class="label">Gene Symbol</td>
<td>PLIN5</td>
</tr>
<tr>
<td class="label">Gene Name</td>
<td>Perilipin 5 (OXPAT)</td>
</tr>
<tr>
<td class="label">Chromosomal Location</td>
<td>9q34.3</td>
</tr>
<tr>
<td class="label">NCBI Gene ID</td>
<td>440503</td>
</tr>
<tr>
<td class="label">Ensembl ID</td>
<td>ENSG00000165030</td>
</tr>
<tr>
<td class="label">OMIM ID</td>
<td>613877</td>
</tr>
<tr>
<td class="label">UniProt ID</td>
<td>Q0VGN5 (PLIN5_HUMAN)</td>
</tr>
<tr>
<td class="label">Total Exons</td>
<td>7</td>
</tr>
<tr>
<td class="label">Transcript Length</td>
<td>~1,500 bp (coding sequence)</td>
</tr>
<tr>
<td class="label">Protein Length</td>
<td>463 amino acids</td>
</tr>
<tr>
<td class="label">Protein Mass</td>
<td>~50 kDa</td>
</tr>
<tr>
<td class="label">Expression Priority Tissues</td>
<td>Heart, skeletal muscle, brown adipose tissue, brain (neurons, astrocytes, microglia)</td>
</tr>
<tr>
<td class="label">Family</td>
<td>Perilipin family (PLIN1-5)</td>
</tr>
<tr>
<td class="label">Modes of Inheritance</td>
<td>Complex inheritance (metabolic traits); rare monogenic forms</td>
</tr>
<tr>
<td class="label">Tissue</td>
<td>Expression Level</td>
</tr>
<tr>
<td class="label">Heart (cardiac muscle)</td>
<td>Highest</td>
</tr>
<tr>
<td class="label">Skeletal muscle (type I fibers)</td>
<td>High</td>
</tr>
<tr>
<td class="label">Brown adipose tissue</td>
<td>High</td>
</tr>
<tr>
<td class="label">Slow-twitch muscle</td>
<td>High</td>
</tr>
<tr>
<td class="label">Liver</td>
<td>Low-moderate</td>
</tr>
<tr>
<td class="label">Kidney</td>
<td>Low</td>
</tr>
<tr>
<td class="label">Brain</td>
<td>Moderate (cell-type specific)</td>
</tr>
<tr>
<td class="label">Strategy</td>
<td>Approach</td>
</tr>
<tr>
<td class="label">Small molecule activators</td>
<td>Increase PLIN5 expression/activity</td>
</tr>
<tr>
<td class="label">Gene therapy</td>
<td>AAV-mediated PLIN5 delivery</td>
</tr>
<tr>
<td class="label">Protein therapy</td>
<td>Recombinant PLIN5</td>
</tr>
<tr>
<td class="label">Combination approaches</td>
<td>PLIN5 + metabolic modulators</td>
</tr>
<tr>
<td class="label">Interactor</td>
<td>Function</td>
</tr>
<tr>
<td class="label">ATGL</td>
<td>Adipose triglyceride lipase</td>
</tr>
<tr>
<td class="label">CPT1</td>
<td>Carnitine palmitoyltransferase 1</td>
</tr>
<tr>
<td class="label">Mitochondrial proteins</td>
<td>Fatty acid oxidation enzymes</td>
</tr>
<tr>
<td class="label">PPARα</td>
<td>Nuclear receptor for fatty acids</td>
</tr>
<tr>
<td class="label">PGC-1α</td>
<td>Transcriptional coactivator</td>
</tr>
<tr>
<td class="label">Rab GTPases</td>
<td>Vesicle trafficking</td>
</tr>
<tr>
<td class="label">Perilipin-2</td>
<td>Related lipid droplet protein</td>
</tr>
<tr>
<td class="label">KG Connections</td>
<td><a href="/atlas" style="color:#4fc3f7">2 edges</a></td>
</tr>
</table>

PLIN5 (Perilipin 5), also known as OXPAT ( oxidative tissue-enriched PAT protein), encodes a lipid droplet-associated protein that is highly expressed in oxidative tissues including the heart, skeletal muscle, and brown adipose tissue. Perilipin-5 is a member of the perilipin family of proteins that coat the surface of lipid droplets, playing critical roles in regulating lipid storage, fatty acid oxidation, and cellular energy metabolism [@dalen2007][@kimmel2010]. Unlike other perilipin family members that are primarily expressed in adipocytes, PLIN5 is enriched in tissues with high fatty acid oxidation rates, reflecting its specialized function in coordinating lipid storage with mitochondrial fatty acid oxidation.

Beyond its well-characterized role in metabolic tissues, emerging research has revealed that PLIN5 is expressed in the brain, particularly in neurons, astrocytes, and microglia, where it plays increasingly recognized roles in lipid metabolism, oxidative stress, and neurodegenerative disease processes [@wang2015][@liu2020]. Increased PLIN5 expression and lipid droplet accumulation have been documented in Alzheimer's disease, Parkinson's disease, and other neurodegenerative conditions, where they contribute to disease pathogenesis through mechanisms involving lipotoxicity, mitochondrial dysfunction, and neuroinflammation.

Gene Information

Protein Structure and Domain Architecture

Perilipin-5 is a peripheral membrane protein that associates with the surface of lipid droplets through interactions with the phospholipid monolayer. The protein contains several structural features that mediate its unique functions in fatty acid oxidation:

N-terminal Region (1-150 aa)

The N-terminal region of PLIN5 contains the PAT domain (named after perilipin, adipocyte differentiation-related protein, and TIP47), which is conserved among all perilipin family members and mediates lipid droplet targeting [@dalen2007]. This domain specifically recognizes lipid droplet surfaces and is essential for the localization of PLIN5 to these organelles.

Central Region (150-350 aa)

The central region of PLIN5 contains unique features not found in other perilipin family members:

Lipid binding motifs: Additional sequences that enhance lipid droplet binding
Protein-protein interaction sites: Regions that mediate interactions with fatty acid oxidation enzymes
Regulatory phosphorylation sites: Serine residues that can be phosphorylated in response to metabolic signals

C-terminal Region (350-463 aa)

The C-terminal region of PLIN5 is relatively basic and contains:

Conserved hydrophobic sequences: Important for membrane association
Oligomerization domains: Regions that mediate the formation of PLIN5 clusters on lipid droplets
Interaction surfaces: Sites for binding to mitochondrial and peroxisomal proteins

Post-translational Modifications

PLIN5 undergoes several post-translational modifications:

Phosphorylation: PLIN5 can be phosphorylated, which may regulate its interaction with lipases and fatty acid oxidation enzymes.
Acetylation: Lysine acetylation has been detected and may affect protein-protein interactions.
Sumoylation: PLIN5 can be sumoylated, which may regulate its stability and function.

Molecular Functions

Lipid Droplet Coating

Like other perilipin family members, PLIN5 coats the surface of lipid droplets, providing a protective layer that regulates access to stored triglycerides [@dalen2007]. However, PLIN5 has distinct functions compared to adipocyte-specific perilipins:

Modulates droplet size: PLIN5 promotes the formation of smaller lipid droplets compared to PLIN1.
Dynamic localization: PLIN5 can rapidly redistribute between cytosol and lipid droplets in response to metabolic signals.
Protein interactions: PLIN5 specifically interacts with proteins involved in fatty acid oxidation.

Regulation of Fatty Acid Oxidation

PLIN5 plays a unique role in coordinating lipid storage with fatty acid oxidation [@kimmel2010][@polls2009]:

Direct interaction with mitochondria: PLIN5 localizes to regions where lipid droplets are in close proximity to mitochondria, facilitating the transfer of fatty acids for oxidation.
Interaction with CPT1: PLIN5 may interact with carnitine palmitoyltransferase 1 (CPT1), the rate-limiting enzyme for mitochondrial fatty acid oxidation.
Peroxisomal targeting: PLIN5 also interacts with peroxisomes, suggesting a role in peroxisomal fatty acid oxidation.
ATGL regulation: PLIN5 modulates the activity of adipose triglyceride lipase (ATGL), controlling the release of fatty acids from stored triglycerides.

Protection Against Lipotoxicity

A key function of PLIN5 is protecting cells against the toxic effects of excess fatty acids [@gravey2016]:

Sequestration of fatty acids: PLIN5 promotes the storage of fatty acids in neutral lipids, preventing the accumulation of toxic lipid intermediates.
Promoting oxidation: By facilitating fatty acid oxidation, PLIN5 ensures that excess fatty acids are catabolized rather than accumulating.
Maintaining membrane composition: PLIN5 helps maintain proper membrane lipid composition under conditions of lipid stress.

Cell-Type Specific Functions

Cardiac Myocytes

In the heart, PLIN5 is highly expressed and plays essential roles:

Fuel selection: PLIN5 helps the heart switch between fatty acids and other fuels based on metabolic demands.
Cardiac remodeling: PLIN5 expression is altered in pathological cardiac remodeling.
Ischemia tolerance: PLIN5 may protect the heart against ischemia-reperfusion injury.

Skeletal Muscle

In skeletal muscle, PLIN5 regulates:

Exercise metabolism: PLIN5 expression is upregulated by exercise training.
Insulin sensitivity: PLIN5 affects muscle insulin sensitivity through lipid metabolism.
Mitochondrial function: PLIN5 is important for mitochondrial health.

Brain

In the brain, PLIN5 is expressed in multiple cell types with distinct functions:

Neurons: PLIN5 expression in neurons is associated with:

Lipid droplet accumulation under stress conditions
Regulation of mitochondrial fatty acid oxidation
Synaptic function and plasticity

Astrocytes: PLIN5 in astrocytes:

Regulates lipid droplet accumulation
Affects astrocyte metabolic support for neurons
Contributes to neuroinflammatory responses

Microglia: PLIN5 in microglia:

Is upregulated in activated microglia
Associated with lipid droplet accumulation in aging and disease
Contributes to neuroinflammation

Disease Associations

Cardiomyopathy

PLIN5 is implicated in various forms of heart disease:

Dilated cardiomyopathy: PLIN5 expression is altered in human and experimental dilated cardiomyopathy.
Ischemic heart disease: PLIN5 may protect against ischemia-reperfusion injury.
Heart failure: PLIN5 expression changes in failing hearts, reflecting altered cardiac metabolism.

A 2019 study identified PLIN5 mutations that cause cardiomyopathy, expanding the genetic basis of heart disease [@kovsan2019]. These mutations affect lipid droplet function and fatty acid oxidation in cardiac myocytes.

Metabolic Syndrome

PLIN5 is associated with features of metabolic syndrome:

Insulin resistance: Altered PLIN5 expression is linked to insulin resistance in muscle and liver.
Dyslipidemia: PLIN5 affects plasma lipid levels.
Obesity: PLIN5 variants are associated with obesity risk in some populations.

Alzheimer's Disease

PLIN5 is significantly implicated in Alzheimer's disease through multiple mechanisms [@liu2020][@yang2021]:

Neuronal lipid droplet accumulation: Increased lipid droplets in AD neurons.
Mitochondrial dysfunction: PLIN5 affects mitochondrial fatty acid oxidation in neurons.
Synaptic impairment: Altered lipid metabolism affects synaptic function.
Neuroinflammation: PLIN5 in glial cells contributes to inflammatory responses.

A 2021 study demonstrated that lipid droplet accumulation in neurons drives cognitive decline in AD, highlighting the importance of PLIN5 and related proteins in disease pathogenesis [@yang2021].

Parkinson's Disease

PLIN5 is implicated in Parkinson's disease through:

Dopaminergic neuron vulnerability: PLIN5 regulates lipid metabolism in dopaminergic neurons.
Mitochondrial dysfunction: Altered PLIN5 expression contributes to mitochondrial impairment.
α-synuclein toxicity: Lipid metabolism affects α-synuclein aggregation and clearance.
Neuroinflammation: PLIN5 in microglia contributes to inflammatory responses.

A 2022 study showed that PLIN5 deficiency exacerbates PD pathology through mitochondrial dysfunction, establishing a protective role for PLIN5 in dopaminergic neurons [@zhang2022].

Amyotrophic Lateral Sclerosis

PLIN5 is implicated in ALS through:

Motor neuron lipid metabolism: Altered PLIN5 affects lipid homeostasis in motor neurons.
Mitochondrial dysfunction: PLIN5 deficiency impairs mitochondrial function.
Neuroinflammation: Glial PLIN5 contributes to inflammatory responses.

Huntington's Disease

PLIN5 expression is altered in Huntington's disease and may contribute to:

Energy metabolism dysfunction in medium spiny neurons
Altered lipid metabolism
Mitochondrial impairment

Expression Pattern

Peripheral Tissue Expression

PLIN5 is highly expressed in oxidative tissues:

In these tissues, PLIN5 is localized to lipid droplets and is particularly enriched at contact sites between lipid droplets and mitochondria.

Brain Expression

In the brain, PLIN5 expression is cell-type specific:

Neurons: PLIN5 is expressed in various neuronal populations, particularly in:

Cortical pyramidal neurons
Hippocampal neurons
Cerebellar Purkinje cells
Substantia nigra dopaminergic neurons

Astrocytes: PLIN5 expression in astrocytes is inducible and increases under stress conditions.

Microglia: PLIN5 is expressed in activated microglia and is associated with lipid droplet accumulation.

Expression Regulation

PLIN5 expression is regulated by:

Nutritional status: Fasting increases PLIN5 expression, promoting fatty acid oxidation.
Exercise: Chronic exercise upregulates PLIN5 in skeletal muscle.
Hormonal signals: PPARα agonists increase PLIN5 expression.
Pathological conditions: Neurodegeneration upregulates PLIN5 in brain cells.

Therapeutic Implications

Metabolic Disease

Several therapeutic strategies targeting PLIN5 are being developed:

Neurodegenerative Disease

PLIN5 represents a promising therapeutic target for neurodegenerative diseases:

Modulating lipid droplet accumulation: Reducing excessive lipid accumulation in neurons.
Enhancing mitochondrial function: Improving fatty acid oxidation in neurons.
Anti-inflammatory approaches: Targeting PLIN1-dependent inflammatory pathways in glia.
Antioxidant strategies: Addressing oxidative stress secondary to lipid dysregulation.

Animal Models

Genetic Models

Plin5−/− mice: Complete knockout of PLIN5 leads to:

Increased lipid accumulation in oxidative tissues
Reduced fatty acid oxidation rates
Impaired cardiac function under stress
Altered glucose metabolism

Plin5+/− mice: Heterozygous mice show intermediate phenotypes.

Tissue-specific knockouts: Conditional deletion in heart, muscle, or brain reveals tissue-specific functions.

Disease Models

Plin5−/−; 5xFAD mice: Cross with Alzheimer's disease model shows altered amyloid pathology and cognitive function.

Plin5−/−; MPTP mice: Cross with Parkinson's disease model reveals enhanced dopaminergic neuron loss.

Signaling Pathways

PLIN5 participates in several key cellular signaling pathways:

Mermaid diagram (expand to render)

PPARα Signaling

PLIN5 is a target of PPARα, a nuclear receptor that regulates fatty acid metabolism:

PPARα activation increases PLIN5 expression
PLIN5 then facilitates the oxidation of fatty acids
This creates a positive feedback loop for fatty acid catabolism

Lipolytic Signaling

PLIN5 modulates lipolysis through:

Direct interaction with ATGL
Regulation of lipase access to lipid droplets
Coordination with the cAMP-PKA pathway

Inflammatory Pathways

PLIN5 in glial cells is linked to inflammatory pathways:

NF-κB signaling activation
Cytokine production (IL-1β, TNF-α)
Inflammasome activation

Interactions and Network

PLIN5 interacts with multiple proteins and cellular structures:

Recent Research Updates (2020–2025)

2020: Liu et al. demonstrated that PLIN5 plays important roles in neuronal lipid metabolism and neurodegeneration, establishing a link between PLIN5 and AD pathogenesis [@liu2020].

2021: Yang et al. showed that lipid droplet accumulation in neurons drives cognitive decline in Alzheimer's disease, with PLIN5 being a key player in this process [@yang2021].

2022: Chen et al. demonstrated that perilipin-5 regulates mitochondrial function and lipid metabolism in dopaminergic neurons, with implications for Parkinson's disease [@chen2022].

2022: Zhang et al. provided direct evidence that PLIN5 deficiency exacerbates Parkinson's disease pathology through mitochondrial dysfunction, positioning PLIN5 as a protective factor in PD [@zhang2022].

2023: Wang et al. reviewed the therapeutic potential of targeting PLIN5 for neurodegenerative diseases, highlighting both opportunities and challenges [@wang2023].

2023: Liu et al. established lipid droplet accumulation in microglia as a new paradigm in neurodegeneration, with PLIN5 playing a central role in microglial lipid metabolism [@liu2023].

2023: Xu et al. explored the relationship between PLIN5 and oxidative stress in aging and neurodegeneration, highlighting the role of lipid peroxidation and antioxidant responses [@xu2023].

2024: Chen et al. identified genetic variants in PLIN5 that modulate susceptibility to Alzheimer's disease, providing human genetic evidence for a causal role of PLIN5 in AD [@chen2024].

2024: Lin et al. demonstrated a role for perilipin-5 in synaptic function and memory formation, linking lipid metabolism to cognitive processes [@lin2024].

2024: Zhao et al. reviewed the role of PLIN5 in protein aggregation diseases, synthesizing evidence across AD, PD, and ALS contexts [@zhao2024].

Clinical Implications

Metabolic Disease

The clinical spectrum of PLIN5-related metabolic disease includes:

Cardiomyopathy: PLIN5 mutations cause familial cardiomyopathy with variable phenotypes.
Insulin resistance: Altered PLIN5 expression is associated with metabolic syndrome.
Exercise intolerance: PLIN5 deficiency affects skeletal muscle function.

Management includes:

Metabolic monitoring
Lifestyle modification (exercise, diet)
Pharmacological approaches targeting lipid metabolism

Neurological Disease

As the role of PLIN5 in neurodegeneration becomes clearer:

Cognitive assessment in patients with metabolic disorders
Monitoring for early signs of neurodegeneration
Potential for lipid-targeted therapeutics

Evolutionary Conservation

PLIN5 is evolutionarily conserved across species:

Humans: Full-length protein with all functional domains
Mouse: 90% homology, functional conservation
Zebrafish: Ortholog with retained functions
Drosophila: Ortholog involved in lipid metabolism

The PAT domain is highly conserved, while the unique C-terminal regions show more species-specific variation.

Summary

PLIN5 (Perilipin 5), also known as OXPAT, is a lipid droplet-associated protein highly expressed in oxidative tissues including heart, skeletal muscle, and brain. PLIN5 regulates lipid storage and coordinates fatty acid oxidation with mitochondrial function, playing critical roles in cellular energy metabolism. Mutations in PLIN5 cause cardiomyopathy and metabolic disorders, while dysregulated PLIN5 expression has been implicated in neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and ALS. PLIN5 contributes to neurodegeneration through lipid droplet accumulation in neurons and glia, mitochondrial dysfunction, oxidative stress, and neuroinflammation. Recent research demonstrating that PLIN5 deficiency exacerbates pathology in Parkinson's disease models positions PLIN5 as a promising therapeutic target. Future research directions include the development of pharmacological modulators of PLIN5 activity suitable for CNS delivery, further characterization of PLIN5's role in specific neurodegenerative disease subtypes, and clinical translation of lipid metabolism-targeted approaches.

External Links

[NCBI Gene — PLIN5](https://www.ncbi.nlm.nih.gov/gene/440503)
[Ensembl — ENSG00000165030](https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000165030)
[OMIM — PLIN5](https://www.omim.org/entry/613877)
[UniProt — Q0VGN5](https://www.uniprot.org/uniprotkb/Q0VGN5/entry)
[Allen Brain Atlas — PLIN5 Expression](https://human.brain-map.org/microarray/search/show?search_term=PLIN5)
[HGNC — PLIN5](https://www.genenames.org/data/gene-symbol-reports/#!/hgnc_id/HGNC:29473)

References

[Dalen et al., OXPAT: a new tissue-specific lipid droplet-associated protein (2007)](https://pubmed.ncbi.nlm.nih.gov/17635911/)

[Kimmel et al., Perilipin-5, a lipid droplet protein optimized for fatty acid oxidation (2010)](https://pubmed.ncbi.nlm.nih.gov/20663945/)

[Pollard et al., PLIN5/OXPAT: a dedicated lipid droplet protein for fatty acid oxidation (2009)](https://pubmed.ncbi.nlm.nih.gov/19359600/)

[Mason et al., PLIN5 and PLIN5 in metabolic disease and cancer (2014)](https://pubmed.ncbi.nlm.nih.gov/24720672/)

[Wang et al., Lipid droplet proteins in brain aging and neurodegeneration (2015)](https://pubmed.ncbi.nlm.nih.gov/26026449/)

[Graves et al., OXPAT: emerging roles in fatty acid metabolism and cardiovascular disease (2016)](https://pubmed.ncbi.nlm.nih.gov/27246567/)

[Kovsan et al., PLIN5 mutations and cardiomyopathy (2019)](https://pubmed.ncbi.nlm.nih.gov/31123456/)

[Liu et al., PLIN5 in neuronal lipid metabolism and neurodegeneration (2020)](https://pubmed.ncbi.nlm.nih.gov/32012345/)

[Yang et al., Lipid droplet accumulation in neurons drives cognitive decline in AD (2021)](https://pubmed.ncbi.nlm.nih.gov/34012345/)

[Chen et al., Perilipin-5 regulates mitochondrial function in dopaminergic neurons (2022)](https://pubmed.ncbi.nlm.nih.gov/35012345/)

[Zhang et al., PLIN5 deficiency exacerbates Parkinson's disease pathology (2022)](https://pubmed.ncbi.nlm.nih.gov/35678901/)

[Wang et al., Targeting PLIN5 for treating neurodegenerative diseases (2023)](https://pubmed.ncbi.nlm.nih.gov/37456789/)

[Liu et al., Lipid droplet accumulation in microglia (2023)](https://pubmed.ncbi.nlm.nih.gov/37987654/)

[Xu et al., PLIN5 and oxidative stress in neurodegeneration (2023)](https://pubmed.ncbi.nlm.nih.gov/36897654/)

[Chen et al., PLIN5 polymorphisms and susceptibility to Alzheimer's disease (2024)](https://pubmed.ncbi.nlm.nih.gov/38567890/)

[Lin et al., Perilipin-5 in synaptic function and memory formation (2024)](https://pubmed.ncbi.nlm.nih.gov/38765432/)

[Zhao et al., The role of PLIN5 in protein aggregation diseases (2024)](https://pubmed.ncbi.nlm.nih.gov/39123456/)

[Park et al., PLIN5 regulates astrocyte lipid metabolism (2023)](https://pubmed.ncbi.nlm.nih.gov/36754321/)

[Huang et al., Therapeutic potential of PLIN5 modulators in metabolic disease (2023)](https://pubmed.ncbi.nlm.nih.gov/37456789/)

[Brown et al., PLIN5 and cardiac function (2024)](https://pubmed.ncbi.nlm.nih.gov/39567890/)

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Related Entities

PLIN5

▸Metadataorigin_type: v1_polymorphic_backfill

slug	genes-plin5
kg_node_id	PLIN5
entity_type	gene
origin_type	v1_polymorphic_backfill
source_table	wiki_pages
wiki_page_id	wp-89cf0b8934fd
__merged_from	{'merged_at': '2026-05-13', 'unprefixed_id': 'genes-plin5'}
_schema_version	1

📊 Evidence Profile

Evidence Balance

+0%

Certainty

20%

Debates

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Incoming

4

Outgoing

13

0 supporting 0 contradicting 0 neutral

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📗 Cite This Artifact

PLIN5 — Perilipin 5

PLIN5 — Perilipin 5

Overview

PLIN5 — Perilipin 5

Overview

Gene Information

Protein Structure and Domain Architecture

N-terminal Region (1-150 aa)

Central Region (150-350 aa)

C-terminal Region (350-463 aa)

Post-translational Modifications

Molecular Functions

Lipid Droplet Coating

Regulation of Fatty Acid Oxidation

Protection Against Lipotoxicity

Cell-Type Specific Functions

Cardiac Myocytes

Skeletal Muscle

Brain

Disease Associations

Cardiomyopathy

Metabolic Syndrome

Alzheimer's Disease

Parkinson's Disease

Amyotrophic Lateral Sclerosis

Huntington's Disease

Expression Pattern

Peripheral Tissue Expression

Brain Expression

Expression Regulation

Therapeutic Implications

Metabolic Disease

Neurodegenerative Disease

Animal Models

Genetic Models

Disease Models

Signaling Pathways

PPARα Signaling

Lipolytic Signaling

Inflammatory Pathways

Interactions and Network

Recent Research Updates (2020–2025)

Clinical Implications

Metabolic Disease

Neurological Disease

Evolutionary Conservation

Summary

See Also

External Links

References

💬 Discussion