Table 2 Introduction to inflammatory vesicles.

From: Targeting mitochondrial autophagy for anti-aging

Protein name

Activation mechanism

Core function

Associated diseases

References

NLRP3

Signals mitochondrial damage: mtDNA leakage, cardiolipin exposure, and reactive oxygen species (ROS) overload.

Other signals: ATP, crystals (uric acid/β amyloid), pathogens

Assembly of ASC-caspase-1 complex, activation of interleukin-1β (IL-1β) \ interleukin-18 (IL-18) induction of cellular pyroptosis

Aging-related: Alzheimer’s disease (Aβ activation),

atherosclerosis (cholesterol crystallization activation) and type 2 diabetes (pancreatic β-cell damage).

Others: gout, CAPS (autoinflammatory syndrome)

[86, 88, 92, 94]

NLRC4

Viral RNA response

Significantly inhibit the activation of NLRP3 and absent in melanoma 2 inflammatory vesicles and reduces the release of IL-1β and IL-18;

promotes autophagy through the beclin-1-dependent pathway

Viral infections: negative regulation of type I interferon response by NLRP4 may result in viruses evading immune clearance;

autoimmune diseases: exacerbates joint inflammation

[157]

NLRP1

Deregulates recombinant dipeptidyl peptidase 8/9 inhibition;

Activates protease cleavage;

directly senses dsRNA

Activates caspase-1 to cleave IL-1β precursor

Activation by Bacillus anthracis triggers immune defenses;

autoimmune disease: hyperactivation of NLRP1 may be associated with chronic inflammation

[158]

AIM2

Directly binds dsDNA

Modulates autoimmune tolerance;

maintains genomic stability;

anti-infection immune defense

Autoimmunity: systemic lupus erythematosus;

infection: HIV infection;

aging-associated: cytoplasmic mtDNA accumulation drives inflammation

[159]

Pyrin

Rho GTPase inactivation in response to bacterial toxins

Immune defense, inflammatory regulation, autoimmune homeostasis

Autoinflammatory diseases: familial Mediterranean fever;

pathogenic infections: salmonella infection

[160]