We propose an extension of the symmetric teleparallel gravity, in which the gravitational action L is given by an arbitrary function f of the non-metricity Q and of the trace of the matter-energy-momentum tensor T , so that L = f (Q, T). The field equations of the theory are obtained by varying the gravitational action with respect to both metric and connection. The covariant divergence of the field equations is obtained, with the geometry-matter coupling leading to the nonconservation of the energy-momentum tensor. We investigate the cosmological implications of the theory, and we obtain the cosmological evolution equations for a flat, homogeneous and isotropic geometry, which generalize the Friedmann equations of general relativity. We consider several cosmological models by imposing some simple functional forms of the function f (Q, T), corresponding to additive expressions of f (Q, T) of the form f (Q, T) = α Q + βT , f (Q, T) = α Q n+1 + βT , and f (Q, T) = −α Q −βT 2. The Hubble function, the deceleration parameter, and the matter-energy density are obtained as a function of the redshift by using analytical and numerical techniques. For all considered cases the Universe experiences an accelerating expansion, ending with a de Sitter type evolution. The theoretical predictions are also compared with the results of the standard CDM model.

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Background: Bone marrow mesenchymal stem cells (BMSCs) exhibit the capacity to self-renew and differentiate into multi-lineage cell types, including osteoblasts, which are crucial regulators of fracture healing. Thus, this study aims to investigate the effect of microRNA (miR)-22-3p from BMSC-derived EVs on osteogenic differentiation and its underlying mechanism. Methods: Extracellular vesicles (EVs) were isolated from BMSCs and taken up with BMSCs. Dual-luciferase reporter gene assay was used to verify the binding relationship between miR-22-3p and FTO. Loss-and gain-of-function experiments were performed to determine the roles of EV-delivered miR-22-3p and FTO in osteogenic differentiation as well as their regulatory role in the MYC/PI3K/AKT axis. To determine the osteogenic differentiation, ALP and ARS stainings were conducted, and the levels of RUNX2, OCN, and OPN level were determined. In vivo experiment was conducted to determine the function of EV-delivered miR-22-3p and FTO in osteogenic differentiation, followed by ALP and ARS staining. Results: miR-22-3p expression was repressed, while FTO expression was elevated in the ovariectomized mouse model. Overexpression of miR-22-3p, EV-delivered miR-22-3p, increased ALP activity and matrix mineralization of BMSCs and promoted RUNX2, OCN, and OPN expressions in BMSCs. miR-22-3p negatively targeted FTO expression. FTO silencing rescued the suppressed osteogenic differentiation by EV-delivered miR-22-3p inhibitor. FTO repression inactivated the MYC/PI3K/AKT pathway, thereby enhancing osteogenic differentiation both in vivo and in vitro. Conclusion: In summary, miR-22-3p delivered by BMSC-derived EVs could result in the inhibition of the MYC/PI3K/ AKT pathway, thereby promoting osteogenic differentiation via FTO repression.