"Sinew prescription correspondence" is the principle of selecting prescriptions for channel sinew diseases. On the basis of the theory of syndrome differentiation and treatment， the pulse manifestation corresponds to the channel sinew syndrome， which can improve the flexibility and standardization of clinical prescriptions. From the perspective of systematic dialectical sphygmology， this paper explains the dialectical relationship between channel sinew theory and pulse body elements， pulse wall elements， pulse elements and blood flow elements， and clarifies the internal relationship between pulse manifestation and prescriptions at the level of channel sinew disease. The prescription is derived from the method， while the method is established with the syndrome， and the prescription is unified by the method. According to the theory of "sinew prescription correspondence"， the treatment ideas of channel sinew diseases were analyzed from the perspective of channel sinew distribution， functional characteristics and structural changes. On this basis， the diagnosis of channel sinew disease and the application of prescriptions are expanded， and the research on the internal treatment and diagnosis mode of "pulse manifestation-channel sinew-zang fu （脏腑）" is prospected， so as to expand the differentiation and treatment methods of channel sinew theory.

Major depressive disorder (MDD) is a common mental disorder characterized by long-term low mood, anhedonia, and may even lead to suicidal behavior. The development and progression of MDD involves a range of pathological alterations in the central nervous system, including dysfunction of synaptic transmission, hyper-activation of neuroinflammation, and diminished neurogenesis. The transient receptor potential vanilloid 1 (TRPV1) channel is highly expressed in brain regions associated with depression, and can regulate physiological activities such as neuroinflammation, neurogenesis, and synaptic transmission efficacy. Hence, the TRPV1 channel should be implicated in the pathogenesis of depression and be considered as a promising candidate for antidepressant treatment. This paper provides an overview of the structure and function of TRPV1 channel, with a focus on elucidating the potential mechanism of action of TRPV1 channel in depression, and explores its research trajectory and development prospects in the context of depression therapy.

Depressive disorder is a kind of mental disorder characterized by persistent and significant depressed mood, with complex etiology and high recurrence rate. At present, more precise and effective diagnostic and therapeutic approaches are still required. Increasing evidence suggests that hypoxia inducible factor-1 (HIF-1) and related pathways are involved in regulating the development and recovery of depression. HIF-1 enhances neuroplasticity, mitigates neuroinflammatory responses, alleviates oxidative stress, and modulates brain energy metabolism by influencing specific molecules associated with depression. This paper reviews pertinent domestic and international studies, examine the potential mechanisms of HIF-1 in the pathogenesis and progression of depression, and explore antidepressant treatment strategies targeting the HIF-1 signaling pathway. This article provides novel insights into elucidating the pathogenesis of depression and developing innovative therapeutic approaches.

Depressive disorder is a kind of mental disorder characterized by persistent and significant depressed mood, with complex etiology and high recurrence rate. At present, more precise and effective diagnostic and therapeutic approaches are still required. Increasing evidence suggests that hypoxia inducible factor-1 (HIF-1) and related pathways are involved in regulating the development and recovery of depression. HIF-1 enhances neuroplasticity, mitigates neuroinflammatory responses, alleviates oxidative stress, and modulates brain energy metabolism by influencing specific molecules associated with depression. This paper reviews pertinent domestic and international studies, examine the potential mechanisms of HIF-1 in the pathogenesis and progression of depression, and explore antidepressant treatment strategies targeting the HIF-1 signaling pathway. This article provides novel insights into elucidating the pathogenesis of depression and developing innovative therapeutic approaches.

Major depressive disorder (MDD) is a common mental disorder characterized by long-term low mood, anhedonia, and may even lead to suicidal behavior. The development and progression of MDD involves a range of pathological alterations in the central nervous system, including dysfunction of synaptic transmission, hyper-activation of neuroinflammation, and diminished neurogenesis. The transient receptor potential vanilloid 1 (TRPV1) channel is highly expressed in brain regions associated with depression, and can regulate physiological activities such as neuroinflammation, neurogenesis, and synaptic transmission efficacy. Hence, the TRPV1 channel should be implicated in the pathogenesis of depression and be considered as a promising candidate for antidepressant treatment. This paper provides an overview of the structure and function of TRPV1 channel, with a focus on elucidating the potential mechanism of action of TRPV1 channel in depression, and explores its research trajectory and development prospects in the context of depression therapy.

Depression is a common debilitating disorder affecting over 300 million individuals worldwide, emphasizing the pressing need to develop novel treatment targets for this disorder. Nevertheless, the pathophysiology of this disorder remains incompletely elucidated, and the currently available antidepressant treatments are suboptimal in terms of their efficacy and delayed onset of action. Thus, identifying and exploring new therapeutic avenues is of paramount importance. Recent clinical and preclinical studies have demonstrated that numerous bitter taste receptor type 2 members (Tas2Rs) agonists, including epigallocatechin gallate (EGCG), resveratrol, caffeine, humulones, and berberine, can significantly alleviate depressive symptoms in both human patients and animal models of depression. However, the precise mechanisms underlying the antidepressant effects of Tas2Rs agonists remain largely unknown. Intriguingly, a growing body of evidence suggests that Tas2Rs agonists may modulate various signaling pathways and systems including neurotransmission, inflammation, brain-gut axis, and the blood-cerebrospinal fluid barrier, all of which are believed to be implicated in the pathophysiology of depression. Therefore, this review aims to provide a comprehensive overview of the potential mechanisms of Tas2Rs agonists in depression, It synthesizes current evidence regarding its involvement in neurotransmission, inflammation, brain-gut communication, blood-cerebrospinal fluid barrier function, and other relevant pathways. This review will not only provide a valuable foundation for future research on the therapeutic potential of Tas2Rs agonists for depressive disorders but also offer new insights into the understanding of the pathophysiology of depression and the development of novel treatment strategies for this disorder.

Major depressive disorder is a common mental disorder with high rate of disability and suicide rate, but its pathogenesis remains unclear. Numerous studies indicate that energy metabolism is impaired in patients with depression, with the changes in the expression of critical genes that regulate mitochondrial homeostasis (mitochondrial biogenesis, fusion and fission, and mitophagy). Mitochondrial dysfunction, leading to reduced ATP production, oxidative stress, and inflammation, plays a significant role in the onset and development of depression, but the mechanism is still uncertain, and conflicting research findings exist. This paper reviews the intrinsic connections and potential mechanism between mitochondrial homeostasis imbalance, dysfunction, and depression, from two aspects: mitochondrial imbalance and dysfunction. It also discusses the limitations of current research, providing insight into understanding the pathogenesis of depression and developing novel mitochondrial-targeted therapeutic strategies.

Depression is a common debilitating disorder affecting over 300 million individuals worldwide, emphasizing the pressing need to develop novel treatment targets for this disorder. Nevertheless, the pathophysiology of this disorder remains incompletely elucidated, and the currently available antidepressant treatments are suboptimal in terms of their efficacy and delayed onset of action. Thus, identifying and exploring new therapeutic avenues is of paramount importance. Recent clinical and preclinical studies have demonstrated that numerous bitter taste receptor type 2 members (Tas2Rs) agonists, including epigallocatechin gallate (EGCG), resveratrol, caffeine, humulones, and berberine, can significantly alleviate depressive symptoms in both human patients and animal models of depression. However, the precise mechanisms underlying the antidepressant effects of Tas2Rs agonists remain largely unknown. Intriguingly, a growing body of evidence suggests that Tas2Rs agonists may modulate various signaling pathways and systems including neurotransmission, inflammation, brain-gut axis, and the blood-cerebrospinal fluid barrier, all of which are believed to be implicated in the pathophysiology of depression. Therefore, this review aims to provide a comprehensive overview of the potential mechanisms of Tas2Rs agonists in depression, It synthesizes current evidence regarding its involvement in neurotransmission, inflammation, brain-gut communication, blood-cerebrospinal fluid barrier function, and other relevant pathways. This review will not only provide a valuable foundation for future research on the therapeutic potential of Tas2Rs agonists for depressive disorders but also offer new insights into the understanding of the pathophysiology of depression and the development of novel treatment strategies for this disorder.

Major depressive disorder is a common mental disorder with high rate of disability and suicide rate, but its pathogenesis remains unclear. Numerous studies indicate that energy metabolism is impaired in patients with depression, with the changes in the expression of critical genes that regulate mitochondrial homeostasis (mitochondrial biogenesis, fusion and fission, and mitophagy). Mitochondrial dysfunction, leading to reduced ATP production, oxidative stress, and inflammation, plays a significant role in the onset and development of depression, but the mechanism is still uncertain, and conflicting research findings exist. This paper reviews the intrinsic connections and potential mechanism between mitochondrial homeostasis imbalance, dysfunction, and depression, from two aspects: mitochondrial imbalance and dysfunction. It also discusses the limitations of current research, providing insight into understanding the pathogenesis of depression and developing novel mitochondrial-targeted therapeutic strategies.

As a common psychiatric disorder, the etiology and pathogenesis of depression are complex and not yet fully elucidated.The diagnosis of depression mainly depends on the patients’ medical history, clinical symptoms and related examinations.Identification of biomarkers will provide important clues for the specific diagnosis and targeted treatment of depression.In addition to the widely recognized neurotransmitter dysregulation, hypothalamus-pituitary-adrenal axis hyperactivity, neuroplasticity, and neuro-inflammation theory, oxidative stress is also involved in the pathogenesis of depression in multiple ways.Many studies showed that the heat shock protein 70(HSP70)levels will increase in early stage to cope with the stress in patients with depression.However, lower HSP70 levels are often correlated with more severe depressive symptoms.HSP70 may be involved in depression through multiple pathways of oxidative stress, glucocorticoid receptors, neuroinflammation and neuroplasticity.Furthermore, increasing HSP70 expression results in significant improvement in depression-like behavior in animals.Thus, HSP70 possesses potential value as an early warning marker for depression as well as a therapeutic target.