Abstract
Heat stress is a major threat to cattle reproduction today. It has been shown that the effect of high temperature not only has a negative effect on the hormonal balance, but also directly affects the quality of oocytes, disrupting the function of mitochondria, fragmenting their DNA and changing their maternal transcription. Studies suggest that the induction of HSP70 may reduce the apoptosis of granular layer cells caused by heat stress. It has been shown that the changes at the transcriptome level caused by heat stress are consistent with 46.4% of blastocyst development disorders. Cows from calves exposed to thermal stress in utero have a lower milk yield in their lifetime, exhibit immunological disorders, have a lower birth weight and display a shorter lifespan related to the expedited aging. In order to protect cow reproduction, the effects of heat stress at the intracellular and molecular levels should be tracked step by step, and the impacts of the dysregulation of thermal homeostasis (i.e., hyperthermy) should be taken into account.
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