Objective To investigate the causes of infertility and its pathogenic mechanism in female SD rats with spontaneous dwarfism (short stature rat, SSR）.Methods Adult wild-type and SSR female SD rats were used for the study. Vaginal smear was used to observe the changes of motile cycle; ovulation promotion was compared using the simultaneous oestrus supernumerary ovulation method; ovarian and uterine weight and body weight, ovarian and uterine indices were measured; AMH, E2, FSH, LH, FSH/LH levels in serum were measured; transcriptomic sequencing of ovarian tissues will be performed to analyze gene expression differences.Results There were no abnormalities in the estrous cycle of SSR female rats., the body weight of SSR female rats was significantly lower than that of wild type, and their ovarian index and uterine index were significantly higher than that of wild type. The mean number of ovulation was significantly higher in wild-type SD rats than in SSR female infertile rats (p<0.001); serum AMH (p<0.01) and E2 (p<0.05) levels were significantly higher in wild-type SD rats than in SSR female infertile rats, and serum FSH (p<0.01), LH (p<0.01) and FSH/LH (p<0.05) The levels of FSH, LH and FSH/LH (p<0.05) were significantly lower in SSR infertile females than in SSR infertile rats, while PROG was not significant; transcriptome sequencing yielded 250 differentially expressed genes, including 190 up-regulated genes and 60 down-regulated genes. p53 signaling pathway and cytokine-cytokine receptor interaction. The MCC, MNC, EPC and Degree calculations of CytoHubba plug-in were used to screen the top 10 significant nodes, respectively, and the intersection was taken to finally obtain 9 Hub genes, namely Cxcl1, Cxcl2, Il1a, Il1b, Cd80, Mmp13, Mmp8, Fgf3 and Ptgs2.Conclusions Infertility in SSR female rats may be related to decreased ovarian reserve function and poor ovarian response. At the same time, Cxcl1, Cxcl2, Il1a, Il1b, Cd80, Mmp13, Mmp8, Fgf3, and Ptgs2 were screened to be associated with infertility, laying a theoretical foundation for further exploration of infertility mechanisms.