The new insights of lactate in various kidney diseases.
Аннотация
BACKGROUND
Kidneys are crucial for systemic lactate homeostasis, and a proper lactate balance subsequently supports normal kidney structure and function. The physiological lactate production-clearance axis along the proximal-distal tubular network may represent an important mechanism for maintaining tubulointerstitial microenvironmental balance. In the context of kidney diseases, the dynamic changes in lactate levels reveal the process of renal metabolic remodelling and even participate in the regulation of disease occurrence and progression.
METHODS
This review systematically combs the maintenance of renal lactate homeostasis under physiological conditions and integrates current research findings on the roles of lactate in the initiation and progression of various kidney diseases, as well as the underlying core molecular mechanisms.
RESULTS
Existing studies confirm that, in a variety of kidney diseases, abnormal lactate levels are closely associated with the occurrence of renal metabolic remodelling, and lactate itself can further regulate the progression of kidney diseases. Targeted regulation of lactate metabolism or lactate-related mechanisms of action is expected to provide a new perspective for the treatment of kidney diseases.
CONCLUSION
The exploration of lactate-related mechanisms offers potential insights for developing novel strategies for early diagnosis and therapeutic intervention of kidney diseases; however, more in-depth studies are still required to translate these findings into clinical practice.
Предметные рубрики MeSH
Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Тип публикации указан по данным источника. Уровень доказательности автоматически не присваивается.