The incidence rate of hypertriglyceridemia pancreatitis (HTGP) has experienced a notable increase in recent years, with eclipsing alcohol as the second leading cause of acute pancreatitis (AP). HTGP is often associated with more severe local and systemic complications. Recognized as a metabolic disorder hypertriglyceridemia (HTG), it holds significant relevance in the pathogenesis of HTGP, yet its mechanisms are not fully understood. Both primary (genetic) and secondary (acquired) factors contribute to elevated triglyceride (TG) levels, which concurrently influence the progression of HTGP. This article presents a comprehensive review of the evolving research on HTGP pathogenesis, encompassing lipid synthesis and metabolism, calcium signal transduction, inflammatory mediators, endoplasmic reticulum stress, autophagy, mitochondrial injury by fatty acids, oxidative stress response, genetic factors, and gene mutations. By unraveling the intricate mechanisms underlying HTGP, this article aims to enhance physicians' understanding of the disease and facilitate the development of potential targeted pharmacological interventions for patients.
Keyphrases
- endoplasmic reticulum stress
- induced apoptosis
- fatty acid
- oxidative stress
- end stage renal disease
- risk factors
- ejection fraction
- genome wide
- chronic kidney disease
- primary care
- liver failure
- transcription factor
- prognostic factors
- drug induced
- physical activity
- early onset
- drug delivery
- risk assessment
- patient reported outcomes
- hepatitis b virus
- human health
- climate change
- mechanical ventilation