Molecular and developmental consequences of heat stress on the bovine oocyte and embryo competence.

Seasonal heat stress (HS) is a pervasive environmental challenge with profound consequences for female reproductive physiology, affecting ovarian function, oocyte maturation, and early embryonic development. At the ovarian level, HS disrupts follicular growth, impairs steroidogenesis, and compromises granulosa cell function, thereby creating a suboptimal microenvironment that reduces oocyte competence. In oocytes, HS induces oxidative stress, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, spindle abnormalities, chromosomal missegregation, and persistent epigenetic alterations. These disruptions extend into early embryonic development, where redox imbalance, apoptosis, ER stress, and altered lineage allocation reduce cleavage and blastocyst formation, compromise trophectoderm and inner cell mass integrity, and impair implantation potential. Maternal heat exposure further exacerbates embryonic vulnerability by altering the oviductal and uterine environment, reducing embryotrophic factors and antioxidant defenses, and ultimately influencing offspring phenotype and fertility, potentially across generations. Accordingly, this review aims to synthesize current knowledge on the physiological and molecular impacts of heat stress on ovarian function, oocyte maturation, and early embryonic development. To this end, we consider studies conducted under both in vivo and in vitro conditions, highlighting shared and distinct mechanisms of thermal stress at the organ and cellular levels to identify potential targets for intervention.