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Heart failure ismainly characterized bymyocardial systolic dysfunction，which is based on excitement-contraction coupling on the cellular level，and calcium (Ca2+ ) signaling plays a very important role in this process. The ryanodine receptor ( RyR) /calcium release channel on the sarcoplasmic reticulum (SR) is the major Ca2+ source of required for cardiac muscle excitation-contraction coupling. RyR2 phosphorylation is the basis of SR calcium release，and RyR2 phosphorylation is mainly controled by protein kinase A (PKA) and calcium/calmodulin dependent protein kinase II (CaMK II ). Although widely research in this area，excessive activation of RyR2 phosphorylation involved in the pathogenesis of heart failure are still controversial which is discussed in this review. [ABSTRACT FROM AUTHOR]

Objective • To explore effects of pCPT-cAMP on proteinurm and dedifferentiation of podocytes in adriamycin (ADR)-induced nephropathy mice. Methods. Male BALB/c mice were divided into three groups. The control group did. not make any intervention, and the other mice were administrated with ADR in a dose of 10 mg/kg by intravenous injection (ADR group). Some ADR-injected mice were treated with pCPT-cAMP [50 mg/(kg-d)] by intraperitoneal injection everyday (A+P group). Albumin urine was detected by Coomassie blue stain. Urine creatinine conceatration was estimated by ELISA. The expression of WT-1 was detected by immuiioliistochemicai staining. IromunofiuoFisscence staining and Western blotting were used to evulate the dedifiereatiation of podocytes. Results • Compared with the control group' the ratio of urinary albiunirt/txeatim&e in ADR nephropathy mice was significantly incteased. WT-1 immuaohistochetaical staiakg showed that tbe number of podocytes was significantly decreased, while immunofluorescence double staining of podocyte-stpecific protein syiuqptopoditi and. podocalyxia remarkably reduced, and tih.e expression of desmin was increased pCPT-«AMP intervention decreased the ratio of albuoun/cKatkime in ADR mice, elevated the quantity of WT-1 positive cells and the expression of syriaptopodin and podocalyxin, while desmin expression decreased. Conclusion • pCPT-cAMP activates the PKA signaling and protects ADR nephropatiiy mice by peventing the loss of podocytes and ameliorating the urine albumin/deatioine ratio, which may be mediated by pCPT-cAMPpreve& ted dedifiTereatiation. of podocytes. [ABSTRACT FROM AUTHOR]

Objective: To observe the effect of electroacupuncture (EA) on urodynamics of neurogenic bladder and pituitary adenylate cyclase activating peptide(PACAP)/cyclic adenosine monophosphate (cAMP)/protein kinase A(PKA) signaling pathway in detrusor tissue of rats after suprasacral spinal cord injury (SCI), so as to explore its possible mechanism in improving detrusor hyperreflexia bladder function after shock stage of suprasacral SCI., Methods: Female SD rats were randomly divided into control, sham operation, model and EA groups, with 12 rats in each group. T10 spinal cord transection (SCT) was performed by surgery. Rats in the EA group were given EA (10 Hz/50 Hz, 20 min) at "Ciliao" (BL32), "Zhongji" (CV3) and "Sanyinjiao" (SP6) once daily for 7 days. After the intervention, urodynamics testing was detected in each group. HE staining was used to observe the morphological changes of bladder detrusor. The protein and mRNA expression of PACAP38 in detrusor was detected by immunohistochemistry, Western blot and real-time quantitive PCR, respectively. The contents of cAMP and PKA were determined by ELISA., Results: Compared with the control and sham operation groups, the maximum bladder capacity and bladder com-pliance, and the protein and mRNA expression of PACAP38, and the contents of cAMP and PKA of the model group were significantly decreased ( P <0.01, P <0.05), while the base pressure and leakage point pressure of bladder were significantly increased ( P <0.01). After EA intervention, the above indexes were all reversed in the EA group relevant to those of the model group ( P <0.01, P <0.05)., Conclusion: EA at BL32, CV3 and SP6 can improve the bladder function in rats with bladder detrusor hyperreflexia after SCI, which may be related to its effect in activating the PACAP/cAMP/PKA signaling pathway in detrusor tissue.

Protein kinase A (PKA) is an important intracellular substance that regulates substance metabolism and biological functions, which exerts a wide range of biological effects through phosphorylation of specific serine/threonine residues in specific proteins. PKA plays an important role in the cAMP signaling pathway, and is involved in various life activities of parasites. Therefore, investigating the role of PKA in the life activities of parasites may provide insights into the development of novel anti-parasitic targets. The review mainly describes the structure and function of PKA and its role in life activities of parasites.