Table 1.

Summary of studies using organoids to model aging.

Type of Organoid	Addressed Hallmark of Aging	Main Findings	Reference
Gut	Stem cell exhaustion; deregulated nutrient sensing	Lower O.F.E.; altered crypt formation	[21,22,23,24,25]
	Epigenetic changes; cellular senescence	Increased senescence markers; altered DNA methylation	[21,26,27]
	Stem cell exhaustion; deregulated nutrient sensing	CR increased O.F.E.; reduced mTOR signaling	[28,29]
	Stem cell exhaustion; deregulated nutrient sensing	NR supplementation increased O.F.E.	[30]
	Altered intercellular communication	Chronic inflammation led to NF-κB activation and cellular transformation	[31]
	Genomic instability	Tissue-specific mutational profile; tumor development	[32,33]
Liver	Genomic instability	Tissue-specific mutational profile; tumor development	[32,34]
Skin	Cellular senescence; altered intercellular communication	Increased senescence markers; decreased ECM synthesis	[35,36,37]
	Cellular senescence; altered intercellular communication	Adipose stem cells prevent skin senescence	[38]
	Altered intercellular communication	Altered TGF-β/Smad signaling	[39]
Tendon	Stem cell exhaustion; cellular senescence; altered intercellular communication	Lower O.F.E; decreased ECM synthesis; increased senescent markers	[40]
Lung	Stem cell exhaustion; cellular senescence; telomer attrition	Lower O.F.E; shortened telomeres; increased senescent markers	[41]
Breast	Genomic instability	Tumor development	[42]
Gastric	Genomic instability; epigenetic changes; altered intercellular communication	PDO characterization; altered Wnt signaling	[43]
Pancreatic	Genomic instability; altered intercellular communication	PDO characterization; altered Wnt signaling	[44]
Brain	Loss of proteostasis	Amyloid plaques and tau aggregates	[45,46]

O.F.E.: organoid formation efficiency; CR: calorie restriction; NR: nicotinamide riboside; ECM: extracellular matrix; PDO: patient-derived organoids.