Autophagy, the process of self-digestion and recycling, plays roles in maintaining cardiac health and responding to various physiological and pathological conditions. In the heart, autophagy helps to preserve cellular homeostasis, adapt to stressors, and prevent the accumulation of damaged components. Its functions range from energy conservation and protein quality control to cardioprotective responses and disease modulation. Autophagy acts as a housekeeping process in adult cardiac cells, removing damaged organelles, misfolded proteins, and other cellular debris. By doing so, it helps to maintain a functional cellular environment and prevent the accumulation of toxic materials that could disrupt cardiac function. Under conditions of nutrient deprivation or energy deficiency, such as during fasting or exercise, autophagy is activated to provide an additional source of energy. By breaking down and recycling cellular components, autophagy generates amino acids and other molecules that can be used for energy production, supporting the heart's contractile function even when external energy sources are limited. Autophagy also plays a role in maintaining the quality of proteins within cardiac cells. It targets damaged or misfolded proteins for degradation, preventing the accumulation of harmful aggregates that could interfere with cellular processes and contribute to cardiac diseases. Autophagy is upregulated the heart in response to various stressors, such as oxidative stress, hypoxia (low oxygen levels), and nutrient deprivation. This heightened autophagic activity helps the heart to adapt to these conditions by removing damaged components and thereby supporting cell survival. It therefore serves as an adaptive response to maintain cardiac function during periods of stress. Autophagy has been further implicated in protecting the heart from damage caused by ischemia (lack of blood flow) and reperfusion injury (restoration of blood flow after ischemia). Inducing autophagy before ischemia can precondition the heart, making it more resistant to subsequent injury. Additionally, autophagy can help mitigate the damage caused by oxidative stress and inflammation. In conditions such as pressure overload-induced hypertrophy, autophagy can also contribute to cardiac remodelling by clearing excess cellular material and supporting the transition to a larger, more efficient heart. However, chronic, or excessive autophagy can also lead to cardiac dysfunction in the long term. Autophagy's role in cardiac diseases is complex and context dependent. In some cases, such as heart failure and cardiomyopathies, excessive autophagy can contribute to the loss of cardiomyocytes and worsen cardiac function. However, in other instances, autophagy can be cardioprotective by removing harmful components and maintaining cellular integrity. Given its diverse roles, autophagy has become a target for potential therapeutic interventions in cardiac diseases. Modulating autophagy can be used to either enhance cardioprotective effects or limit excessive autophagy that may lead to detrimental outcomes. Researchers are exploring drugs and interventions that can finely tune autophagy to achieve optimal outcomes in different cardiovascular conditions. For example, trehalose is a naturally occurring disaccharide and potential autophagy enhancer. It promotes autophagic flux thereby helping to remove damaged cellular components, and some preclinical studies have suggested potential benefits in protecting the heart from stress-induced damage. We provide a large product catalogue of research tools for studying autophagy, including LAMP2 antibodies, Sumo 1 antibodies, ULK1 antibodies, Apg12 antibodies, and Bag1 antibodies. Explore our full autophagy product range below and discover more, for less. Alternatively, you can explore our APG Gene Products and Autophagosome product ranges.