Table 1.

Supplementation with NAD ⁺ precursors improve ovarian aging and fertility outcomes.

Intervention	Species	Mechanisms	Fertility outcomes	Ref
NMN	Mice	rescues of the NADH/NAD redox state in oocytes damaged by mtDNA mutations	improved the first litter rate	[36]
	Mice	protects the first meiosis and reduces spindle assembly defects and the incidence of aneuploidy	oocyte quality, follicle dynamics, embryo development, and live birth rates were recovered	[32]
	Mice	restores meiotic maturation in aged oocytes, improves mitochondrial function, reduces ROS levels, and inhibits DNA damage and apoptosis	enhanced sperm binding ability of aged oocytes, improved fertilization ability, and early embryonic development of aged oocytes	[37]
	Mice	up-regulates the level of mitochondrial metabolism and autophagy, increases the antioxidant capacity of follicles, and reduces oxidative damage	improved endocrine function, increased follicular reserve, and delayed fertility decline	[38]
	Mice	improves mitochondrial function and oxidative stress, reduces DNA damage and early apoptosis	–	[39]
	Pig	enhances mitochondrial function and inhibits oxidative stress-induced apoptosis	improved the fertilization rate of aged oocytes	[40]
	Pig	restores meiotic defects, enhances mitochondrial function, and inhibits ROS, DNA damage, and apoptosis	promoted oocyte development and early embryonic development	[41]
	Pig	restores mitochondrial function eliminates excess ROS, and rescues meiotic defects	–	[42]
NR	Mice	improves mitochondrial function	increased ovulation potential and live birth rate	[31]
	Mice	reduces ROS levels, DNA damage, and apoptosis	improved fertilization potential and embryo development potential	[43]
NA	Mares	improves maternal age-related meiotic defects	oocyte-matured blastocysts contain more cells	[34]
	Mice	improves maternal age-related meiotic defects and oocyte oxidative stress	–	[44]
	Mice	inhibits apoptosis	–	[45]
	Pig	–	improve blastocyst formation rate	[46]
NAM	Pig	–	blastocysts contain more cells	[46]
	Mice	inhibits fragmentation and spindle elongation and minimizes acetylation of α-tubulin during oocyte senescence	–	[47]
	Mice	reduces ROS levels and oxidative stress	promoted oocyte maturation and improved fertilization rate	[48]