Recent work shows that gut dysbiosis fuels systemic inflammation that impairs endometrial stromal cell decidualization and promotes senescence, while senescent stromal cells reinforce dysbiosis via SASP-mediated alterations in gut permeability and immune signaling. We hypothesize that a specific class of microbial metabolites—secondary bile acids produced by dysbiotic strains such as Clostridium scindens and Bacteroides fragilis—directly modulates the senescence-associated secretory phenotype (SASP) of endometrial stromal fibroblasts through inhibition of histone deacetylases (HDAC1/2), leading to hyperacetylation of NF‑κB p65 and sustained transcription of pro‑inflammatory SASP factors (IL‑6, IL‑8, MCP‑1, CXCL10). This HDAC inhibition also reduces expression of the decidualization‑critical gene SPTLC1, linking microbial metabolism directly to the stromal defect observed in RIF‑M patients. Conversely, SASP‑derived extracellular vesicles enriched in miR‑34a, miR‑146a, and miR‑21 are released by senescent endometrial stromal cells, travel via the circulation, and are taken up by gut epithelial cells and resident microbiota. These miRNAs suppress bacterial genes required for SCFA biosynthesis (e.g., the butyrate kinase gene buk in Faecalibacterium prausnitzii and the propionate‑producing pathway in Akkermansia muciniphila), thereby decreasing luminal butyrate and propionate levels. The resulting SCFA deficit diminishes GPR43‑mediated anti‑inflammatory signaling in intestinal macrophages, increasing gut permeability and allowing more microbial bile acids to reach the uterine microenvironment, closing the loop. This self‑reinforcing circuit predicts three testable outcomes: (1) endometrial stromal cells exposed to physiologically relevant concentrations of deoxycholic acid will show increased SASP secretion and reduced SPTLC1 expression, an effect reversible by HDAC inhibition with trichostatin A; (2) intravenous injection of endometrial‑derived extracellular vesicles from aged mice will lower fecal SCFA concentrations and decrease abundance of butyrate‑producing taxa in recipient young mice, accompanied by heightened serum LPS‑binding protein; (3) combined pharmacological inhibition of intestinal bile‑acid reabsorption (cholestyramine) and senolytic clearance of p21high endometrial stromal cells (using navitoclax) will synergistically restore fecal butyrate, reduce endometrial IL‑6 staining, and improve decidualization markers (IGFBP1, PRL) in naturally aged female mice, whereas each monotherapy yields only partial rescue. Experimental validation could employ aged C57BL/6 females treated with cholestyramine chow, navitoclax intraperitoneal dosing, or both, followed by endometrial single‑cell RNA‑seq to assess SASP and decidualization signatures, fecal metabolomics for SCFAs, 16S rRNA sequencing for microbiota shifts, and functional implantation assays after embryo transfer. Falsification would occur if bile‑acid modulation fails to alter endometrial SASP or if senescent cell clearance does not rescue SCFA‑producing microbes despite reduced stromal senescence.